Lub Leaky Gut Thiab Lub plab Microbiome hauv Sepsis Lub Hom Phiaj Hauv Kev Tshawb Fawb Thiab Kev Kho Mob
Nov 21, 2023
Ob lub plab hnyuv (ib qho teeb meem ntawm lub plab zom mov) thiab plab dysbiosis (ib qho kev hloov hauv plab hnyuv microbial) yog qhov tseem ceeb rau sepsis. Thaum sepsis nws tus kheej tuaj yeem ua rau dysbiosis, dysbiosis tuaj yeem ua rau mob sepsis. Cov kab mob plab hnyuv xau yog hais txog cov xwm txheej uas muaj cov plab hnyuv permeability ntxiv uas tso cai rau kev hloov pauv ntawm microbial molecules los ntawm plab hnyuv mus rau hauv cov ntshav. Nws tsis yog ib qho tsos mob ntawm kev mob plab hnyuv, tab sis kuj yog ib qho laj thawj uas tshwm sim ntawm nws tus kheej, thiab nws lub xub ntiag tuaj yeem raug lees paub los ntawm kev kuaj pom, hauv cov ntshav, ntawm lipopolysaccharides thiab (1 → 3)- -D-glucan (qhov tseem ceeb Cheebtsam ntawm plab microbiota). Gut-dysbiosis yog qhov tshwm sim ntawm kev txo qis hauv qee hom kab mob hauv plab microbiome, raws li qhov tshwm sim ntawm plab hnyuv mucosal tiv thaiv kab mob, tshwm sim los ntawm plab hnyuv hypoperfusion, lub cev tiv thaiv kab mob apoptosis, thiab ntau yam enteric neuro-humoral-immunity teb. Kev txo qis ntawm cov kab mob uas tsim cov roj ntsha luv luv tuaj yeem hloov cov kab mob hauv plab hnyuv, ua rau kev hloov pauv ntawm cov kab mob molecules, mus rau hauv txoj kev uas nws ua rau muaj kab mob. Txawm tias lub plab fungi tuaj yeem nce ntxiv hauv tib neeg cov neeg mob uas muaj sepsis, txawm tias qhov no tsis tau pom zoo nyob rau hauv cov qauv murine ntawm sepsis, tej zaum vim lub sijhawm ntev ntawm sepsis thiab kuj siv tshuaj tua kab mob hauv cov neeg mob. Lub plab microbiome uas ib nrab muaj cov kab mob bacteriophages tseem tuaj yeem kuaj tau hauv plab cov ntsiab lus uas tej zaum yuav txawv ntawm sepsis thiab cov tswv tsev ib txwm muaj. Cov kev hloov pauv ntawm plab dysbiosis tag nrho tuaj yeem yog lub hom phiaj nthuav dav rau kev kho mob sepsis adjuvant, piv txwv li, los ntawm kev hloov fecal lossis kev kho probiotic. Ntawm no, cov ntaub ntawv tam sim no ntawm cov plab hnyuv thiab plab dysbiosis nrog rau cov peev txheej biomarkers, cov tswv yim kho tshiab, thiab cov ncauj lus tshawb fawb yav tom ntej tau hais.
cistanche ntxiv cov txiaj ntsig-kho cem quav
Taw qhia
Sepsis yog ib hom mob uas muaj kev tuag siab thiab mob [1]. Txawm hais tias tsis ntev los no tau txo qis hauv sepsis cov neeg tuag, sepsis tseem suav txog kwv yees li 20% ntawm cov neeg tuag thoob ntiaj teb, nrog rau 60% kev tuag ntawm cov neeg mob septic shock [2,3]. Cov kab mob kab mob no feem ntau ua rau mob sepsis, tab sis feem ntau ntawm cov chaw kho mob tshwm sim ntawm cov kab mob hnyav tshwm sim los ntawm cov kab mob, fungi, kab mob, thiab kab mob parasitic, xws li leptospirosis, aspergillosis, dengue shock syndrome, thiab mob malaria hnyav, zoo li xav tsis thoob, thiab. suav nrog cov hlab plawv tsis ua haujlwm, ua rau cov ntshav siab tsawg thiab cov nqaij tsis zoo perfusion, lub raum raug mob, ua rau anuria, thiab pulmonary dysfunction, ua rau hypoxemia [4-7]. Cov kev zoo sib xws no qhia txog kev ua haujlwm ntawm lub cev tiv thaiv kab mob tseem ceeb hauv lub cev, piv txwv li, kev tiv thaiv kab mob sai, tsis yog kev tiv thaiv kab mob, piv txwv li, cov lus teb lig [8]. Lub luag hauj lwm ntawm microbial molecules tsis tsim los ntawm tus tswv tsev (pathogen-associated molecular patterns [PAMPs]) thiab molecules los ntawm tus tswv tsev lub hlwb (kev puas tsuaj-kho cov qauv molecular [DAMPs]) yog txawv los ntawm kev tiv thaiv kab mob hauv lub cev los ntawm kev tiv thaiv innate thaum lub sij hawm sepsis [9] . Ib qho kev tiv thaiv kev tiv thaiv kab mob, orchestrated los ntawm T thiab B lymphocytes, nrog rau cov tshuaj tiv thaiv, yog qhov tseem ceeb sib npaug [10]. Qee qhov PAMPs thiab DAMPs nrog cov peev txheej thiab cov qauv kev lees paub tseem ceeb tau teev tseg hauv Table 1 [11–13]. Qhov tseem ceeb ntawm PAMPs nyob rau hauv sepsis implicates gastrointestinal ib ntsuj av tau raws li ib tug endogenous reservoir ntawm ob peb pawg ntawm cov kab mob, xws li prokaryotes, piv txwv li, kab mob thiab archaea, eukaryotes, piv txwv li, fungi, thiab kab mob, feem ntau bacteriophages, uas yog sib koom ua ke hu ua ' plab microbiota. '. Cov kab mob no tau sib cais los ntawm tus tswv tsev los ntawm tsuas yog ib txheej ntawm enterocytes uas muaj cov kab nrib pleb nruj [14,15]. Thaum lub sij hawm sepsis, enterocytes muaj hyperpermeability tshwm sim los ntawm ntau yam, nrog rau plab hnyuv hypoperfusion, enterocyte apoptosis, ib tug systemic cytokine cua daj cua dub, thiab plab dysbiosis, uas yuav txhawb txoj kev hloov ntawm microbial molecules los ntawm lub plab mus rau hauv lub cev. Qhov no feem ntau hu ua 'cov plab hnyuv ntxwm' [16,17], uas yog ib qho tseem ceeb uas yuav cuam tshuam nrog kev txhim kho kab mob hauv ntau yam mob, nrog rau kev ua ub ua no tsis tu ncua (kev tawm dag zog, ntau cov kua txob, qee yam tshuaj thiab kev ntxhov siab. ) [18–20] lossis kab mob (cov kab mob autoimmune, kab mob, rog, thiab uremia) [21–24]. Muaj qhov sib txawv hauv cov kab mob pathophysiology ntawm cov plab hnyuv hauv cov kab mob no. Piv txwv li, lub plab permeability puas nyob rau hauv lub cev lupus erythematosus (ib hom kab mob autoimmune) yog tshwm sim los ntawm kev tiv thaiv kab mob hauv lub plab thiab qhov tsis zoo ntawm qee cov tshuaj, suav nrog cov tshuaj uas tsis yog tshuaj tiv thaiv kab mob (NSAIDs), corticosteroids, thiab kab mob- Hloov kho cov tshuaj tiv thaiv kab mob (DMARDs) [14]. Lub caij no, qhov kev ntxhov siab vim kev ntxhov siab hauv plab yog tshwm sim los ntawm kev ntxhov siab hormone-vim lub cev tsis muaj zog hloov pauv nrog lub paj hlwb autonomic (lub plab-hlwb axis) [25] thiab ob qho tib si cuam tshuam ntawm lupus thiab kev ntxhov siab thaum kawg ua rau plab dysbiosis thiab plab hnyuv. Kev txhim kho plab permeability uas txaus txaus kom tso cai rau kev hloov pauv ntawm cov kab mob uas siv tau, thiab tshwj xeeb tshaj yog qee cov kab mob nkag mus, los ntawm lub plab mus rau lub cev, tuaj yeem ua rau mob sepsis, feem ntau hu ua 'Gut-derived sepsis' [26, 27] ib. Lub microbiota, kev tiv thaiv hauv zos, thiab kev ncaj ncees hauv plab yog qhov tseem ceeb rau kev saib xyuas lub plab microenvironment; Yog li ntawd, kev tswj hwm ntawm cov xwm txheej no yuav muaj txiaj ntsig zoo hauv kev kho mob sepsis. Txawm hais tias muaj kev paub ntau ntxiv ntawm cov plab hnyuv thiab plab dysbiosis hauv sepsis, cov chaw kho mob txhais cov ntaub ntawv no rau cov neeg mob tseem tsawg heev. Txawm hais tias kev hloov pauv ntawm cov kab mob hauv plab thaum lub sij hawm sepsis yog qhov paub zoo, kev tshawb nrhiav ntawm sepsis-vim hloov pauv hauv cov kab mob fungi thiab kab mob hauv plab tsis ntev los no tau nce ntxiv uas tuaj yeem nthuav tawm qhov nthuav dav tshiab. Tom qab ntawd, kev sau cov ntaub ntawv tam sim no ntawm cov ncauj lus no tuaj yeem pab txhawb kev txaus siab rau kev siv qee qhov kev txwv thiab kev kho mob hauv kev kho mob tiag tiag. Yog li ntawd, qhov kev tshuaj xyuas no nthuav qhia txog qhov muaj feem cuam tshuam ntawm lub plab microbiome, hais txog cov kab mob, cov kab mob, thiab cov kab mob, ntawm cov kab mob sepsis, thiab tshawb nrhiav tam sim no npaj cov kev kho mob ntxiv, suav nrog kev hloov fecal lossis kev kho probiotic.
Table 1 Common PAMPs thiab DAMPs hauv sepsis
Lub plab zom mov ua rau muaj cov microbial molecules nyob rau hauv cov hlab ntsha
Ib txheej ntawm cov hlwb epithelial nrog thaj tsam ntawm thaj tsam li 32 m2 kab ntawm lub plab zom mov (GI) nto thiab tuav ua ke los ntawm cov kab mob epithelial nruj junctions (TJs). Cov txheej txheem no ua haujlwm ua thawj theem ntawm kev tiv thaiv kab mob hauv lub cev thiab ua haujlwm raws li kev xaiv lub cev tiv thaiv ntawm tus tswv tsev thiab microbial molecules [28,29]. TJ complex tsis tso cai rau kev nkag mus ntawm cov molecules loj dua 3.6 ˚ A lossis 0.6 kDa los ntawm cov kab ke ib txwm muaj (qhov chaw nruab nrab ntawm qhov sib thooj ntawm enterocytes). Cov molecules loj dua raug thauj mus los ntawm lub plab epithelial hlwb los ntawm ntau cov txheej txheem transcytosis, suav nrog clathrin-mediated endocytosis, micropinocytosis, thiab caveolin-mediated endocytosis [30,31]. Qee cov microbial-derived molecules, xws li p-cresol (lub plab-derived uremic toxin muab los ntawm cov protein fermentation los ntawm cov kab mob plab), me me txaus kom dhau los ntawm lub plab barrier [32], whereas lwm cov molecules, xws li lipopolysaccharide (LPS. ) los ntawm cov kab mob Gram-negative thiab (1→3)- -D-glucan (BG) los ntawm cov kab mob fungi (cov kab mob ntau tshaj plaws thiab thib ob tshaj plaws hauv plab) lossis microbial DNA, loj dhau los hla qhov thaiv [ 33] ib. Txawm li cas los xij, txawm hais tias cov kab mob DNA loj loj (piv txwv li, cov genome) nrog qhov loj me ntawm 100 txog 15, 000 kilobase khub (kbp) (6.5 × 104-9.8 × 106 kDa) loj dhau los hla lub plab barrier. , DNA molecules tau tawg sai sai rau hauv cov kab mob DNA tsis muaj kab mob los ntawm ntau cov txheej txheem (depurination thiab deamination) rau hauv daim kwv yees li 100 bp (65 kDa) hauv qhov loj (piv txwv li qhov loj me rau LPS thiab BG) [34]. Yog li, kev tshawb pom ntawm cov PAMPs (LPS, BG, thiab cov kab mob tsis muaj DNA) tuaj yeem yog cov cim qhia tsis ncaj ntawm lub plab. Xwb, kev tswj hwm qhov ncauj ntawm cov carbohydrates uas tsis nqus tau thiab nws qhov kev tshawb pom tom qab hauv cov ntshav lossis zis yog qhov kev kuaj pom zoo rau lub plab [35,36]. Txawm li cas los xij, qhov tsim nyog ntawm kev tswj hwm qhov ncauj thiab cov plab hnyuv peristalsis txwv kev siv cov txheej txheem no tsuas yog rau cov neeg mob uas tsis muaj mob.
Kev raug mob plab hauv zos nrog thaj chaw loj ntawm qhov chaw tsis yog qhov xav tsis thoob ua rau lub plab zom mov, raws li pom hauv cov nas uas tau kho nrog cov tshuaj dextran sulfate tsawg (DSS), ib yam khoom uas ua rau TJ raug mob. Cov tsos mob ntawm plab hnyuv loj hlob los ntawm asymptomatic mus rau raws plab [37] los yog mob pancreatitis nrog endotoxemia [38]. Nyob rau tib lub sijhawm, PAMPs muaj ntau ntau pom hauv cov ntshav, suav nrog hauv DSS-tswj nas, yog cov cim qhia ntawm lub plab [39]. Interestingly, lub plab hnyuv hauv DSS-tswj nas yog pom tau tias muaj fluorescein isothiocyanate (FITC)-dextran assay. Hauv tib neeg, kev tshawb pom ntawm qee cov carbohydrates uas tsis nqus tau hauv cov zis tom qab kev tswj hwm qhov ncauj tau pom, txawm tias tsis muaj tsos mob plab (zaum raws plab lossis qhov quav tsis zoo sib xws) [40], txhais tau tias muaj peev xwm asymptomatic leaky plab. Xws li, qhov kev xav tam sim no yog tias lub plab zom mov (cov plab hnyuv tsis muaj qhov cuam tshuam loj)" yuav tshwm sim, raws li tau pom hauv cov ntshav microbiome tshuaj ntsuam nrog muaj DNA los ntawm cov kab mob plab anaerobic uas feem ntau tsis muaj nyob hauv cov ntshav. [34]. Txawm hais tias muaj ntau ntawm DNA nyob rau hauv cov ntshav ntawm kev noj qab haus huv cov nas yog tsawg heev los yog tsis-detectable, cov DNA amplification txheej txheem siv nyob rau hauv bacteriome tsom xam yuav ntes tau tsawg npaum li cas ntawm DNA. Qhov tseem ceeb, cov txheej txheem kho tsis tu ncua ntawm 'physiologic leaky plab' yuav tsum tsis txhob tsim cov plab hnyuv fibrosis vim qhov tseem ceeb ntawm tus kheej rov ua dua tshiab ntawm cov enterocytes [41]. Txawm li cas los xij, plab hnyuv fibrosis tuaj yeem tsim tau nyob rau hauv cov ntaub ntawv ntawm qhov mob hnyav hnyav raws li qhia hauv kab mob plab hnyuv (ulcerative colitis) [42]. Cov ntaub ntawv pov thawj ntxiv rau lub cev lub cev xau plab yog qhov kuaj pom cov ntshav BG hauv qee cov neeg noj qab haus huv, tshwj xeeb tshaj yog nrog Fungitel assay (Associates of Cape Cod, Inc.), vim tias BG yog ib qho tseem ceeb ntawm cov kab mob uas yog txawv teb chaws molecule rau tus tswv tsev, nrog rau qhov ib txwm muaj (tsawg dua 60 pg / ml) uas muaj peev xwm ua rau muaj kev cuam tshuam lub plab hauv cov neeg noj qab haus huv (nrhiav cov ntshav BG yam tsis muaj kev puas tsuaj) [17,35,36]. Raws li xws li, BG yog lub ntuj polysaccharide uas muaj cov kab ke D-glucose moieties txuas los ntawm -(1 ntawm qhov chaw, xws li BG los ntawm fungi yog tsim los ntawm → 3)-glycosidic bonds nrog rau lwm yam qauv ntawm ntau yam nyob ntawm -(1 → 6)- txuas ceg los ntawm -(1→3) qaum [43]. Cov kev cuam tshuam ntawm BG, tshwj xeeb tshaj yog kev sib koom ua ke nrog LPS, feem ntau hais txog [44–48].
Los ntawm qhov sib txawv, endotoxemia yuav tsum tsis txhob raug kuaj pom hauv tus tswv tsev noj qab haus huv, txawm tias muaj qhov ua tau qis ntawm cov plab hnyuv, tej zaum yog vim muaj ntau yam LPS neutralization ua, xws li deacylation thiab dephosphorylation los ntawm acyl-oxy-acyl hydrolase thiab alkaline phosphatase, raws li [49- 51] ib. Qhov tseem ceeb, tsis muaj cov tshuaj tiv thaiv enzymatic rau BG neutralization [52]. Yog li, LPS thiab BG hauv cov ntshav, thaum tsis muaj lwm qhov chaw pom tseeb, yog qhov nthuav tawm cov plab hnyuv biomarkers uas muaj txiaj ntsig zoo dua rau kev siv tshuaj kho mob piv nrog tus qauv kev tswj hwm qhov ncauj carbohydrate. Txawm li cas los xij, qib ntawm LPS thiab BG hauv cov ntshav tsis yog nyob ntawm qhov hnyav ntawm lub plab khoob tab sis kuj cuam tshuam nrog cov kab mob Gram-negative thiab fungi hauv plab. Hauv cov qauv tsiaj, ntau yam mob ua rau muaj kab mob Gram-negative (Bacteroides thiab Proteobacteria) thiab tej zaum LPS hauv plab cov ntsiab lus, suav nrog sepsis, DSS-induced mucositis, uremia, rog, thiab fungal tswj [39,48,53-55. ], thaum muaj cov ntsiab lus txhim kho ntawm fecal fungi (thiab BG) hauv plab yog ua tau tom qab siv tshuaj tua kab mob, mob plab hnyuv (mob plab hnyuv; IBD), thiab haus cawv [44,45,56–58]. Yog li, siv qhov muaj pes tsawg leeg ntawm LPS thiab BG los txiav txim siab qhov hnyav ntawm lub plab zom mov yog qhov nyuaj; Txawm li cas los xij, lawv yuav muaj txiaj ntsig zoo rau qhov qhia tau tias lub plab barrier puas tsuaj.
Kev soj ntsuam lub plab khoob tsis yog qhov xav tsis thoob tom qab mob plab lossis mob raws plab los ntawm ib qho laj thawj (kev kis kab mob, cov kab mob tiv thaiv kab mob, thiab DSS) [53,59–61] vim yog kev puas tsuaj ncaj qha rau TJ. Txawm li cas los xij, pathophysiology ntawm cov kab mob uas ua rau lub plab ua rau lub plab tuaj yeem cuam tshuam rau cov kab mob paracellular enterocyte permeability (raws li qhia los ntawm LPS cov qauv txhaj tshuaj) [62] thiab / los yog kev ntxhov siab vim lub plab dysbiosis [63,64]. Qhov tseeb, LPS txhaj tshuaj ua rau tsim cov ntshav cytokines, uas tuaj yeem cuam tshuam rau txhua lub cell hauv lub cev, suav nrog enterocytes, thiab cytokine activation ua rau enterocyte kev ncaj ncees, raws li pom los ntawm kev txo qis transepithelial hluav taws xob tiv thaiv hauv enterocytes tom qab incubation nrog pro-inflammatory cytokines [65] . Tsis tas li ntawd, neuro-hormonal cuam tshuam los ntawm kev teb rau kev ntxhov siab (thiab kev nyuaj siab), tshwj xeeb tshaj yog kev txhim kho ntawm catecholamine, tuaj yeem hloov cov kab mob hauv plab, ib feem, vim yog catecholamine hlau chelation uas pab txhawb kev loj hlob ntawm cov kab mob hlau-metabolizing [66. ]. Kev ua haujlwm ntawm enteric neurons los ntawm corticotropin-tso yam hauv lub cev tiv thaiv kab mob (macrophages thiab mast cells) kuj tuaj yeem hloov kho microbial tswj mechanism hauv plab [67]. Nws tseem yog qhov nthuav kom nco ntsoov tias muaj qhov sib npaug ntawm cov lus teb tiv thaiv kab mob, hu ua 'cov tshuaj tiv thaiv kab mob tiv thaiv kab mob', thaum lub sijhawm ua haujlwm hyper-inflammatory hauv cov kab mob loj heev, tshwj xeeb tshaj yog nyob rau hauv sepsis, qhov tsis txaus ntseeg homeostasis ntawm kev tiv thaiv kab mob zoo li. txhawm rau ua rau muaj kev mob siab rau septic shock lossis lub cev tsis muaj zog (ib qho ntxiv rau kev kis tus kabmob thib ob) [68–70] uas tuaj yeem ua rau muaj kev raug mob enterocyte thiab cov plab hnyuv, tej zaum, nrog cov txheej txheem sib txawv. Xav paub ntau ntxiv txog lub ncauj lus no yuav nthuav.
Cov teebmeem ntawm cistancetubulosa- Kho cem quav
Lub plab thiab plab dysbiosis
Qhov sib npaug ntawm tus tswv tsev tiv thaiv kev ua ub no thiab cov kab mob hauv lub plab ua rau lub plab microbiota tshwj xeeb hauv cov tswv tsev sib txawv raws li cov tshuaj tiv thaiv kab mob hauv lub cev thiab lub plab microenvironmental yam (kev noj haus thiab kev ua ub no) yuav txawv ntawm tib neeg. Yog li, kev hloov pauv ntawm kev tiv thaiv kab mob hauv lub cev, vim kev laus, tshuaj tua kab mob, khoom noj, lossis qhov pib tshiab ntawm qee cov kab mob hauv lub cev tuaj yeem ua rau muaj kev hloov hauv plab microbiota [71–73]. Piv txwv li, qhov depletion ntawm macrophages los yog splenectomy hauv tus tswv tsev txo cov kev ua haujlwm microbicidal tawm tsam qee cov kab mob hauv plab ua rau lub plab dysbiosis [64,74] thiab cov kev xaiv microbicidal ntawm cov tshuaj tua kab mob sib txawv ua rau qee qhov sib txawv dysbiosis hauv tus tswv [75,76]. Hauv qhov sib piv, lub plab dysbiosis tuaj yeem ua rau qee qhov kev hloov pauv hauv lub cev tiv thaiv kab mob uas muaj feem cuam tshuam rau txoj hnyuv. Raws li xws li, plab dysbiosis tshwm sim los ntawm qhov ncauj tswj hwm ntawm cov kab mob pathogenic lossis cov kab mob fungi pab txhawb kev cuam tshuam ncaj qha ntawm enterocytes thiab ua kom lub cev tiv thaiv kab mob ua rau lub plab hnyav dua li qhov muaj nyob hauv tus tswv tsev nrog cov kab mob tsis zoo [37,45,77. ]. Qhov tseem ceeb, muaj cov kab mob hauv plab hloov cov kab mob hauv plab los ntawm ntau lub tswv yim, xws li kev xaiv cov kab mob uas tuaj yeem zom tau qee cov molecules ntawm cov phab ntsa ntawm tes los yog cov kab mob uas muaj cov kab mob fungal toxin resistance [39,74]. Yog li, kev tiv thaiv kab mob, ob qho tib si hauv zos plab hnyuv tiv thaiv kab mob thiab kev tiv thaiv kab mob hauv lub cev, cuam tshuam rau plab dysbiosis thiab vice versa thiab tuaj yeem ua rau muaj kev cuam tshuam hauv plab hnyuv (leaky plab) los ntawm kev puas tsuaj los ntawm kev tiv thaiv kab mob (enterocytes yog cov neeg sawv cev ntawm microbicidal kev tiv thaiv) thiab / lossis los ntawm invasiveness ntawm pathogenic microbes.
Thaum lub sij hawm sepsis, muaj kev hloov pauv hauv lub cev tiv thaiv kab mob thiab lub plab dysbiosis nrog ntau yam sepsis uas txhim kho plab hnyuv tsis raug. Rau sepsis-induced lub cev tiv thaiv kab mob, hyper-inflammatory cytokines, kev tuag ntawm lub cev tiv thaiv kab mob los ntawm lub cev tiv thaiv kab mob, thiab kev nyuaj siab hormone-activated plab hnyuv tiv thaiv [8,78,79] yuav cuam tshuam rau qhov qub tshuav ntawm tus tswv tsev tiv thaiv kab mob thiab microbes. Hauv sepsis-induced plab dysbiosis, muaj ntau ntawm cov kab mob siab heev hauv plab thaum lub sij hawm sepsis tuaj yeem nce ntxiv vim tias cov kab mob no feem ntau muaj ntau yam cuam tshuam rau qhov hnyav microenvironment, thaum ib txwm microbiota feem ntau pom tias tsis muaj cov xwm txheej no [80]. Ntxiv mus, ntau qhov tsis xws luag thaum lub sij hawm sepsis, piv txwv li, plab hypoperfusion los ntawm cov kab mob vasodilatation thiab / los yog sepsis-induced cardiomyopathy, plab hnyuv hypomotility, thiab plab mucosal cuam tshuam [81] kuj ncaj qha ua rau lub plab tsis xws luag thiab plab hnyuv. Yog li ntawd, enterocyte hyperpermeability nyob rau hauv sepsis yog tshwm sim los ntawm ntau yam, xws li plab hnyuv hypoperfusion, enterocyte apoptosis, systemic cytokine cua daj cua dub, thiab plab dysbiosis uas yuav txhawb txoj kev hloov ntawm microbial molecules los ntawm lub plab mus rau hauv cov ntshav ncig (gut lossis plab to) [16 , 17] ib. Txawm hais tias endotoxemia thiab circulating cell-free DNAs (cf-DNAs) pom nyob rau hauv cov kab mob sepsis tej zaum yuav muab tau los ntawm cov kab mob tuag hauv cov ntshav, qee cov LPS molecules tej zaum yuav cuam tshuam nrog translocation ntawm lub plab mus rau hauv cov ntshav ncig (gut translocation). Cov pov thawj zoo dua ntawm lub plab khoob thaum lub sij hawm sepsis los ntawm qhov muaj endotoxemia thiab glycemia (serum BG) yam tsis muaj kab mob bacteremia thaum lub sij hawm kis kab mob, xws li pom muaj tus kab mob dengue thiab tus kab mob coronavirus 2019 (COVID-19) nrog cov kab mob hnyav [35, 82–84] ib. Txawm hais tias muaj kev sib xyaw ntawm cov kab mob sib xyaw ua ke tuaj yeem ua tau, tshuaj tua kab mob (thiab tshuaj tiv thaiv kab mob) tsis tsim nyog rau feem ntau ntawm cov neeg mob uas muaj tus kab mob viral sepsis. Tsis tas li ntawd, kev tswj hwm ntawm cov kab mob lysate kuj muaj cov kab mob DNA thaum lub sij hawm lub plab induction los ntawm DSS hauv cov nas nce qib ntawm cf-DNAs hauv cov ntshav [34], implying lub plab translocation thaum lub sij hawm sepsis. Ib qho kev tshawb pom nthuav yog tias lub plab khoob tuaj yeem yog qhov ua rau thiab / lossis qhov tshwm sim ntawm cov kab mob sepsis vim (i) cov kab mob plab hnyav ua rau muaj cov kab mob hloov pauv tau thiab cov kab mob bacteremia, raws li qhia los ntawm DSS-induced sepsis [64,77], thiab ( ii) kev puas tsuaj rau enterocyte TJ thaum lub sij hawm sepsis ua rau lub plab zom mov [45]. Nyob rau hauv ob qho tib si, lub plab khoob yuav txhim kho cov kab mob hauv lub cev los ntawm kev tiv thaiv kab mob hauv lub cev, tshwj xeeb tshaj yog los ntawm macrophages thiab neutrophils [40,46,85]. Ib yam li ntawd, plab dysbiosis (qhov tsis txaus ntawm plab microbiota cuam tshuam nrog qhov tshwm sim tsis zoo) tuaj yeem ua rau thiab / lossis qhov tshwm sim ntawm cov kab mob sepsis vim qhov tseem ceeb ntawm plab microbiota hauv kev saib xyuas txoj hnyuv [86].
Tam sim no, ntau txoj hauv kev (ntau-qab zib sojntsuam, LPS, BG, thiab lwm yam molecules) [87] muaj rau kev ntsuas lub plab, tab sis ua cov kev ntsuas no thaum lub sij hawm sepsis yog qhov nyuaj vim muaj kev txwv hauv kev tswj hwm qhov ncauj rau cov neeg mob hnyav, Qhov sib txawv ntawm LPS thiab BG nyob rau hauv lub plab cov ntsiab lus, Gram-negative bacteremia (uas txwv tsis pub siv LPS raws li cov pa paug hauv plab) thiab qhov tsis paub meej kev kho mob ntawm ntau cov molecules (zonulin, fatty acid binding protein, thiab lwm yam) . Vim tias muaj kev cuam tshuam rau lub plab khoob thaum lub sij hawm sepsis, ib qho kev ntsuam xyuas ntau ntawm cov plab hnyuv yuav tsis tsim nyog, thiab cov kev ntsuam xyuas zoo rau cov plab hnyuv (xws li BG) nrog cov ntsuas dysbiosis (xws li kev nplua nuj ntawm Firmicutes, Bacteroides, thiab Proteobacteria los ntawm microbiome kev tsom xam lossis cov tshuaj tiv thaiv kab mob polymerase [PCR]) yuav tsim nyog rau kev siv tshuaj kho mob. Txawm hais tias qhov sib txawv ntawm cov tsiaj uas kuaj pom los ntawm kev tshuaj xyuas microbiome yog cov ntaub ntawv ntau dua, qhov sib txawv ntawm cov qib phylum siv PCR nrog cov primers xaiv yuav tsis tshua kim thiab tsim nyog rau kev siv tiag tiag. Muaj kev tshawb fawb ntxiv ntawm lub ncauj lus no tau lees paub.
Cov kab mob plab hnyuv microbiome
Vim tias cov kab mob yog cov kab mob tseem ceeb tshaj plaws hauv plab, feem ntau ntawm ' plab dysbiosis' tau hais hauv cov kev tshawb fawb feem ntau hais txog kab mob dysbiosis. Lub plab microbiota ib txwm muaj xws li qhov tseem ceeb ntawm Firmicutes (Bacillota) (feem ntau yog cov kab mob Gram-positive nrog obligate aerobes lossis facultative anaerobes) thiab Bacteroides (feem ntau yog Gram-negative anaerobes uas yog cov kab mob hauv qee qhov xwm txheej) [88]. Firmicutes yog cov kab mob tseem ceeb tshaj plaws hauv lub plab noj qab haus huv, ib feem ntawm kev hloov pauv ntawm cov carbohydrates nyuaj rau hauv cov saw hlau luv fatty acids (SCFAs, tshwj xeeb tshaj yog butyrate), uas yog ib qho tseem ceeb ntawm kev loj hlob ntawm lub plab epithelium. Bacteroides yog cov kab mob Gram-tsis zoo tshaj plaws hauv plab thiab tej zaum sawv cev rau qhov loj ntawm LPS hauv txoj hnyuv [89]. Qhov piv ntawm Firmicutes / Bacteroides tuaj yeem ua tus biomarker rau kev noj qab haus huv ntawm lub plab barrier, vim qhov no qis dua hauv ntau yam mob, suav nrog kev kis kab mob, DSS colitis, post-splenectomy, macrophage depletion, rog rog, uremia, hlau overload thiab sepsis [24] ,48,55,77,90,91], thiab qhov nce Firmicutes/Bacteroides piv tau qhia hauv IBD [92,93]. Txawm hais tias muaj txiaj ntsig ntawm SCFA ntau lawm los ntawm cov kab mob Firmicutes feem ntau (xws li cov kab mob probiotic ntawm lactobacilli thiab enterococci), qee pawg (xws li cov kab mob ntawm cov kab mob clostridial) yog cov kab mob uas yuav ua rau lub plab puas tsuaj [94,95]. Ib yam li ntawd, ntau hom kab mob Bacteroides muab cov khoom noj rau lwm tus neeg nyob hauv microbial thiab txo cov kab mob hauv plab, txawm tias muaj peev xwm ua tau rau lwm cov Bacteroides [88]. Proteobacteria (Pseudomonadota), ib lub cev loj ntawm cov kab mob Gram-tsis zoo (nrog rau ntau yam kab mob), yog lwm cov kab mob phylum uas nquag pom tias nce ntxiv thaum lub plab dysbiosis [96-98]. Yog li, ob qho tib si nce thiab txo qis hauv Firmicutes / Bacteroides piv nrog nce Proteobacteria qhia plab dysbiosis; Txawm li cas los xij, ntau cov kev tshawb fawb tau lees paub ua ntej siv qhov piv txwv no rau kev siv tshuaj kho mob.
Lub plab microbiota ib txwm muaj qhov cuam tshuam rau microenvironment, raws li kev tswj hwm ntawm qhov ncauj ntawm cov kab mob lossis cov kab mob ua rau lub plab zom mov los ntawm kev nce hauv cov kab mob pathobionts [37,45], thaum lub plab xau vim DSS induces dysbiosis los ntawm plab mucosal o [53]. Txoj hnyuv o tuaj yeem yog lwm yam uas ua rau lub plab dysbiosis, raws li kev tswj hwm qhov ncauj ntawm Candida albicans hauv kev tswj cov nas tsis hloov cov kab mob fecal microbiota, thaum C. Albi cov kaus poom gavage hauv cov nas septic tom qab cecal ligation thiab puncture (CLP) phais lossis DSS- colitis nce qhov feem ntawm Gammaproteobacteria (ib pawg ntawm cov kab mob pathogenic, suav nrog Pseudomonas aeruginosa) [39,53]. Tseeb tiag, plab hnyuv mob los ntawm ntau yam ua rau, suav nrog qee cov khoom noj (cov khoom noj muaj rog), cov tshuaj (cov tshuaj uas tsis yog steroidal anti-inflammatory, NSAIDs), thiab kev ntxhov siab (kev tawm dag zog hnyav), tuaj yeem txo cov mucin ntau lawm (mucin barrier) thiab nce tus lej. ntawm cov kab mob pro-inflammatory (thiab cov neeg nruab nrab), uas ua rau muaj kev xaiv ntawm qee pawg kab mob uas tiv taus ntau dua rau kev tiv thaiv kab mob (feem ntau yog cov kab mob uas muaj kab mob loj heev) [18,19,99–101]. Hloov pauv, qhov txo qis hauv kev tiv thaiv kab mob, xws li macrophage depletion, kuj tseem tuaj yeem ua rau qee cov kab mob uas tau tswj los ntawm plab hnyuv macrophages thiab ua rau plab dysbiosis [74].
Cov txiaj ntsig ntawm cistanche tubulosa
Vim muaj qhov tsis zoo ntawm lub plab microbiota, qee tus cwj pwm ntawm tus tswv tsev yuav raug muab cais raws li cov yam ntxwv tsis zoo sepsis. Qhov no tuaj yeem tshwm sim hauv cov tib neeg uas muaj cov kab mob SCFA uas tsim tawm qis dua, cov caj ces tsis muaj peev xwm ntawm cov plab hnyuv ib txwm muaj (ua rau cov mucin thiab cov tshuaj tiv thaiv kab mob peptides; AMPs), lossis hauv cov neeg uas tsis muaj zaub mov noj lossis kev tiv thaiv kab mob, vim cov quav microbiome yog ib qho rhiab biomarker rau cov mob no [102,103]. Piv txwv li, Mucin 2 tsis muaj peev xwm (Muc2-/-) nas tsim colitis thaum muaj hnub nyoog 6 hli, nrog kev nce hauv Firmicutes/Bacteroidetes thiab qee cov Proteobacteria (Desulfovibrio thiab Escherichia) [104]. Ib qho tsis xws luag hauv AMPs tau hais hauv IBD-induced dysbiosis [105], thiab cov menyuam yaus uas muaj kev noj zaub mov tsis zoo ua rau pom cov Proteobacteria nce ntxiv thiab txo cov Bacteroides hauv quav [106,107]. Yog li ntawd, kev txo qis hauv Firmicutes lossis qis Firmicutes / Bacteroides piv yuav yog qhov qhia txog tus lej ntawm SCFA-ua cov kab mob tsawg thiab tuaj yeem sawv cev rau tus yam ntxwv ntawm kev nkag mus rau lub plab-derived sepsis vim tias lub plab yooj yim cuam tshuam ntawm cov kab mob pathogenic [93,108]. Txawm li cas los xij, kev kuaj pom cov kab mob tsis zoo hauv cov tib neeg noj qab haus huv yuav tsis yog qhov tseem ceeb hauv kev kho mob vim tias muaj lwm yam kev tiv thaiv tsis zoo (xws li mucin thiab kab mob hauv plab). Tsis tas li ntawd, cov kab mob hauv nruab nrog cev los ntawm lub plab tsis tu ncua, txawm tias mob hnyav, yuav raug cuam tshuam sai sai los ntawm ntau cov txheej txheem zoo ib yam li cov tshwm sim hauv lub plab physiological leaky plab. Yog li ntawd, kev ntsuas ntawm lub plab khoob ntawm ob peb lub sij hawm cov ntsiab lus yuav tsim nyog los txheeb xyuas tus neeg sawv cev thiab cov chaw kho mob cov plab hnyuv loj hauv cov neeg mob tiag tiag, vim qhov no yuav txawv ntawm cov qauv tsiaj uas tsis tshua muaj kev hloov pauv hauv cov xwm txheej. Peb qhov kev sim tau qhia tias tus kab mob bacteriosis nyob rau hauv qee cov nas mob uremic tom qab 48 h ob sab nephrectomy yog tshwm sim los ntawm txoj hnyuv apoptosis, uas ua rau mob hnyav heev [90], rov hais txog qhov tseem ceeb ntawm lub plab barrier. Txawm hais tias qhov kev twv ua ntej ntawm sepsis susceptibility los ntawm plab dysbiosis ib leeg, lossis tej zaum los ntawm kev txo qis hauv Firmicutes (los yog nce hauv Bacteroides thiab Proteobacteria) yam tsis muaj kev ntsuas lub plab, tej zaum yuav muab cov ntaub ntawv txwv, ob peb tsab ntawv ceeb toom txhawb qee qhov kev kwv yees ntawm dysbiosis. Piv txwv li, kev depletion ntawm Rosburia (phylum Firmicutes) thiab nce hauv Prevotella (Phylum Bacteroides) hauv plab yog txheeb xyuas qhov muaj feem cuam tshuam rau kev mob stroke-mob ntsws thiab mob ntsws ntsws ntev (COPD), feem [109,110], thaum nce hauv Kleicolaribsiella. thiab Enterobacteriaceae (phylum Proteobacteria) yog txuam nrog sepsis cardiomyopathy [111]. Qhov tseem ceeb, qee cov kab mob metabolites, feem ntau tau los ntawm kev zom cov as-ham (xws li polyamines), me me kom dhau los ntawm cov kab mob hauv plab; Txawm li cas los xij, qhov cuam tshuam ntawm cov molecules hauv sepsis tsis meej npaum li qhov loj dua microbial molecules (LPS, BG, thiab cf-DNA) [112,113].
Nyob rau hauv sib piv rau lub plab tsis muaj teeb meem nyob rau hauv dysbiosis ua ntej sepsis, sepsis coj ncaj qha mus rau lub plab dysbiosis ua ke nrog rau cov plab hnyuv leaky thiab tso cai rau translocation ntawm microbial molecules los yog siv tau cov kab mob. Kev hloov pauv microbial los ntawm lub plab feem ntau yog cov kab mob ntau dua li cov kab mob fungi (Candida spp.), vim qhov loj ntawm cov kab mob fungi dua li cov kab mob. Txo cov hnyuv perfusion tuaj yeem pom tau nyob rau theem pib ntawm sepsis nrog cov ntshav siab (ua ntej poob siab), txawm tias lub cev vasodilatation (distributive shock) thiab myocardial depression (ib feem ntawm hyper-cytokinesis) [114,115], los ntawm kev txo qis hauv plab microcirculation. raws li qhia los ntawm sepsis-induced ileus [116]. Vim tias ileus tuaj yeem yog qhov cim ntxov ntawm kev mob plab, xws li los ntawm kev kis kab mob (sepsis) lossis tsis muaj kab mob (ntau raug mob lossis ntau lub cev tsis ua haujlwm; MOF), tab sis nthuav tawm nrog cov ntshav siab, qhov txo qis hauv plab hauv sepsis thiab MOF yuav tshwm sim. ntxov heev nyob rau hauv tej yam ntuj tso kab mob [117]. Ntawm ntau yam cuam tshuam nrog sepsis-induced plab hnyuv disorders [81], plab hypoperfusion yog ib qho tseem ceeb uas tej zaum yuav ua rau (i) enterocyte puas (necrosis thiab apoptosis) nrog rau cov plab hnyuv thiab (ii) plab hnyuv tiv thaiv kab mob (kev tuag ntawm lub cev tiv thaiv kab mob. ) nrog txo qis microbial tswj kev ua haujlwm thiab nce plab dysbiosis (kev xaiv tsuas yog cov kab mob uas muaj kab mob siab heev). Sepsis yog nrog los ntawm apoptosis ntawm txhua lub cev tiv thaiv kab mob (neutrophils, macrophages, dendritic cells, thiab lymphocytes), nyob rau hauv ib feem, vim muaj kev tiv thaiv kab mob los ntawm ob qho tib si PAMPs los ntawm cov kab mob thiab kev puas tsuaj cuam tshuam nrog cov qauv molecular (DAMPs) tshwm sim los ntawm kev tuag ntawm lub cev lub cev [118] Lub cev tiv thaiv kab mob apoptosis no yog ib qho ntawm cov txheej txheem uas ua rau lub cev tsis muaj zog (lub peev xwm txo qis los tiv thaiv lwm yam kab mob, ua rau muaj kab mob thib ob) [119]. Sepsis kuj ua rau muaj kev ua haujlwm tsis zoo hauv ntau lub cev (lub raum, siab, ntsws, tus po, thiab lub paj hlwb) thiab kev puas tsuaj rau txhua lub cev tuaj yeem cuam tshuam rau plab dysbiosis. Piv txwv li, lub raum thiab lub siab puas tsuaj thaum lub sij hawm sepsis yuav ua rau lub excretion ntawm accumulated metabolites (toxins) rau hauv lub plab, thiab cov no yuav ncaj qha cuam tshuam rau enterocytes thiab txhawb kev loj hlob ntawm ib co kab mob (xws li cov kab mob uas muaj peev xwm metabolize cov co toxins), uas ua rau lub raum thiab lub siab puas. dysbiosis nrog rau plab hnyuv [90,120]. Ib yam li ntawd, sepsis tuaj yeem hloov kho lub cev tiv thaiv kab mob, xws li kev tshem tawm ntawm lub ntsws uas tsim tawm hom I interferons, uas tuaj yeem hloov kho lub plab microbiome [121], yog li tuaj yeem txo tus lej ntawm cov kab mob anaerobic thiab nce qhov feem ntawm Proteobacteria [122]. Ib yam li ntawd, kev hloov pauv ntawm neuro-immuno-endocrine axis thaum lub sij hawm sepsis kuj tseem cuam tshuam rau plab dysbiosis [113]. Yog li, sepsis induces plab dysbiosis los ntawm kev cuam tshuam ntawm plab hypoperfusion, tiv thaiv kab mob, thiab lub cev tsis ua haujlwm. Interestingly, qee qhov zoo sib xws yog pom tseeb ntawm sepsis uas tshwm sim los ntawm ntau qhov sib txawv ntawm tus kab mob. Qhov no yog vim, ib feem, rau ntau yam ntawm cov mob hnyav thiab nyob rau hauv cov kab mob inflammatory teb, nrog rau kev poob ntawm cov kab mob uas muaj txiaj ntsig thiab kev sib txawv ntawm cov kab mob microbial thiab kev nce hauv cov kab mob [123,124]. Piv txwv li, fecal microbiota nyob rau hauv cov menyuam yaus uas muaj kab mob sepsis muaj cov kab mob ntau dua (Acinetobacter thiab Enterococcus) nrog cov kab mob uas muaj txiaj ntsig tsawg (Roseburia, Bacteroides, Clostridia, Faecalibacterium, thiab Blautia), thiab cov kev hloov pauv no cuam tshuam nrog cov yam ntxwv kho mob tab sis qhia txog kev koom tes tsis zoo nrog. Lub sijhawm ntawm cov tshuaj tua kab mob [125]. Ib yam li ntawd, qhov depletion ntawm Lachnospiraceae, Ruminococcaceae, thiab Ruminococcus thiab kev txhim kho ntawm Enterococcus tau pom nyob rau hauv kev tshuaj xyuas ntawm cov kab mob sepsis [126]. Kev kis kab mob hnyav (COVID-19, mob npaws, thiab dengue) kuj tuaj yeem ua rau cov kab mob nce ntxiv, tshwj xeeb tshaj yog cov kab mob Gram-negative, thaum lub sij hawm sepsis thiab pab txhawb lub plab translocation ntawm LPS (endotoxemia) los yog cov kab mob siv tau (bacteremia), nyob ntawm qhov xau. lub plab hnyav, uas ua rau qhov mob hnyav zuj zus ntxiv [127–129] (Daim duab 1).
Daim duab 1. Kev hloov pauv ntawm tag nrho cov kab mob (cov kab mob, cov kab mob, thiab phages) koom nrog hauv sepsis thiab lub plab tiv thaiv kab mob Sepsis induces plab hnyuv tiv thaiv kab mob, los ntawm txoj hnyuv hypoperfusion (vasodilatation thiab cardiomyopathy), immune cell apoptosis, kev ntxhov siab hormone (corticotropin) / enter -induced lub cev tiv thaiv kab mob, thiab kab mob o, inducing plab dysbiosis (sab laug sab). Nyob rau tib lub sijhawm, sepsis-induced plab dysbiosis, tshwm sim los ntawm plab hnyuv tiv thaiv kab mob, tshuaj tua kab mob, thiab kev hloov pauv hauv cov kab mob fungi thiab phages, ua rau lub plab translocation ntawm microbial molecules los yog cov kab mob uas siv tau (cov plab hnyuv) ua rau mob plab (sab xis) uas ua rau lub plab tsis zoo thiab ua rau lub plab tsis zoo. plab dysbiosis raws li ib tug vicious voj voog. Daim duab tau tsim los ntawm BioRender.com.
Lub plab hnyuv mycobiome
Txawm hais tias qhov loj ntawm cov fungi (10}-12 μm; Candida poov xab) dua li cov kab mob (0.5-2 μm), cov kab mob yog qhov thib ob uas muaj kab mob hauv plab. Yog li ntawd, qhov kev nplua nuj (los ntawm cov ntawv theej) yog 1000-fold ntau dua rau cov kab mob (16S rRNA) dua li cov kab mob (18S rRNA), nrog ntau dua 3,500 hom kab mob piv nrog 267 hom kab mob hauv plab [29]. Cov kab mob hauv zej zog sib txawv hauv qhov ntau thiab muaj pes tsawg leeg los ntawm lub plab mus rau txoj hnyuv (102 vs 1011 hlwb / gram cov ntsiab lus hauv plab thiab txoj hnyuv, raws li), hos cov fungi zoo li nyob hauv zos feem ntau hauv cov nyuv, nrog qhov nruab nrab ntawm 106 fungal hlwb ib. gram ntawm txoj hnyuv loj [130] Feem ntau cov kab mob plab hnyuv mycobiota hauv cov neeg noj qab haus huv yog los ntawm phyla Ascomycota (63%) (tshwj xeeb yog Candida albicans) thiab Basidiomycota (32%) [131], thiab cov overgrowth ntawm C. albicans feem ntau pom nyob rau hauv cov neeg mob uas muaj kab mob sepsis tshwm sim hauv ib feem. rau tshuaj tua kab mob xaiv siab [132]. Candida colonization nyob rau hauv lub plab kuj yog ib qho tseem ceeb txaus ntshai rau cov kab mob candidiasis tom qab kab mob sepsis [133]. Tseeb, Candida colonization nyob rau hauv lub plab muaj ntau heev nyob rau hauv cov neeg mob nyob rau hauv intensive care units (ICUs +) [134,135], thiab Candida translocation ntawm lub plab mus rau hauv cov ntshav ncig yog ua tau thaum cov kab mob sepsis [136,137]. Vim tias qhov qis dua ntawm cov kab mob hauv cov quav nas dua li hauv tib neeg cov quav (zoo kab lis kev cai yog yooj yim pom hauv tib neeg), kev tswj hwm ntawm C. albicans rau nas yog siv los tshawb txog qhov tseem ceeb ntawm Candida hauv sepsis. Txawm hais tias nws qis dua, qhov muaj Candida hauv plab txhim kho qee hom kab mob (xws li Pseudomonas spp.) [44,53], ib nrab vim glucan digestion, raws li kev sib xyaw glucan rau hauv kab lis kev cai nruab nrab txhawb kev loj hlob ntawm cov kab mob sib cais [39 ]. Interestingly, cov fungal-bacterial kev sib cuam tshuam yog complex thiab tej zaum yuav nyob ntawm seb lub sij hawm ntawm qhov raug, raws li incubation ntawm ib tug soj ntsuam hom ntawm Pseudomonas aeruginosa nrog C. albicans tsis muaj synergy ntawm biofilm ntau lawm, whereas ntxiv cov fungi mus rau Pseudomonas biofilms. los yog kab xov tooj ntawm tes pab txhawb ntau biofilm ntau lawm [138,139]. Txawm li cas los xij, kev nce hauv Candida hauv plab thaum lub sijhawm sepsis tuaj yeem ua rau qhov hnyav ntawm cov kab mob sepsis los ntawm ntau txoj hauv kev, suav nrog kev hloov pauv ntau dua ntawm BG (Candida nce BG lub plab cov ntsiab lus), nce cov kab mob hauv plab, thiab ncaj qha raug mob rau enterocytes ( Tej zaum los ntawm cov kab mob Candida los yog mucosal tiv thaiv kab mob tiv thaiv kab mob) [44,77]. Qhov tshwj xeeb tshaj yog, kev nthuav qhia ntawm LPS thiab BG synergistically activates macrophage immune teb, nyob rau hauv ib feem los ntawm kev ua kom ib txhij ntawm TLR-4 thiab dectin-1 los ntawm LPS thiab BG, feem [45,46,85].
cistanche cov txiaj ntsig rau txiv neej-ua kom muaj zog tiv thaiv kab mob
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Txawm hais tias tsis muaj cov ntaub ntawv hais txog lub plab mycobiota hauv cov neeg mob sepsis, septic nas qhia hloov maj mam hloov hauv plab fungi (qhov ntau ntawm fungal 18sRNA los ntawm PCR hauv sepsis yog txawv ntawm pawg tswj), suav nrog kev txo qis ntawm Myrothecium spp. fungi uas tuaj yeem tsim qee cov molecules tawm tsam ntau yam teeb meem (qee yam kab mob thiab tshuaj lom) [15]. Qhov sib txawv ntawm cov kab mob sepsis ntawm tib neeg thiab cov nas [140,141] nce qhov ua tau tias cov kab mob plab hauv cov neeg mob sepsis tuaj yeem txhim kho los ntawm ntau yam sib txawv ntawm cov nas, xws li lub sijhawm sepsis (tib neeg cov neeg mob muaj sia nyob ntev dua nas), Kev siv tshuaj tua kab mob (muaj zog ntau dua hauv tib neeg lub cev), chav saib xyuas mob hnyav (ICU) ib puag ncig (cov kab mob nosocomial zoo li hauv cov neeg mob hauv ICUs dua li cov nas hauv cov chaw tswj tsiaj) thiab ntau dua Candida hauv tib neeg quav thiab kab mob hauv qab (xws li hloov plab hnyuv. fungi nyob rau hauv hom 2 mob ntshav qab zib) [142–144]. Raws li kev txhim kho zoo hauv plab fungi nyob rau hauv cov neeg mob nrog IBD thiab haus cawv [56-58], plab hnyuv o thiab txo mucosal tiv thaiv tej zaum yuav yog ib qho tseem ceeb exacerbating yam rau kev txhim kho plab fungi txuam nrog sepsis (systemic cytokine-induced plab hnyuv barrier. tsis xws luag thiab apoptosis ntawm lub cev tiv thaiv kab mob) [65,118]. Kev tshawb nrhiav ntau dua ntawm plab fungi hauv cov neeg mob uas muaj kab mob sepsis yuav nthuav. Nco ntsoov, kev txheeb xyuas ntawm mycobiota nyob rau theem phylum tsuas yog muab cov ntaub ntawv txwv vim tias Ascomycota predominate; Yog li ntawd, kev soj ntsuam fecal microbiome tej zaum yuav tsim nyog los tshawb nrhiav cov kab mob fungal hauv cov quav.
Lub plab hnyuv microbiome
Tam sim no, cov kab mob hauv plab tsis suav nrog 'mob plab microbiota', vim cov kab mob yog cov kab mob hauv lub cev thiab muaj cov kab mob hauv enterocytes yuav raug cais raws li tus kab mob kis. Txawm li cas los xij, cov kab mob bacteriophages, uas yog cov kab mob (lossis genomes) ntawm cov kab mob plab, tej zaum yuav raug suav hais tias yog ib pawg ntawm cov kab mob uas tuaj yeem pom hauv plab cov ntsiab lus thiab categorized li ' plab microbiota' vim tias kev hloov pauv hauv cov kab mob plab yuav hloov pauv ntau ntawm cov kab mob bacteriophages. (los yog phages). Phaages yog tshwj xeeb rau hom kab mob, ib feem vim yog txoj kev sib txawv ntawm kev nkag, thiab phages ntawm tib cov kab mob yuav muaj cov lus teb sib txawv rau cov kab mob sib txawv [145]. Piv txwv li, cov phages muaj txiaj ntsig tiv thaiv P. aeruginosa los ntawm Tus Neeg A yuav tsis muaj txiaj ntsig rau P. aeruginosa los ntawm tus neeg B. Qhov no yuav tsum muaj ntau yam ntaub ntawv phage (phage tsev qiv ntawv) rau kev siv tshuaj kho mob tiag tiag [146]. Lub voj voog bacteriophage tau muab faib ua lysogenic thiab lytic qauv. Lub voj voog lysogenic cuam tshuam nrog kev tso cov khoom siv tshuaj tua kab mob rau hauv cov kab mob genome rau kev rov ua dua ua ke nrog cov kab mob. Cov phages no raug xa mus rau 'temperate phages lossis prophages' thiab tuaj yeem hloov mus rau ntau tiam kab mob yam tsis muaj kab mob kis kab mob. Los ntawm qhov sib txawv, lub voj voog lytic yog hloov los ntawm lysogenic theem mus rau kev tso tawm cov kab mob tshiab [147,148]. Vim tias phages yog ib qho kev tswj hwm ntuj tiv thaiv kab mob [149] thiab vim hais tias prophages tuaj yeem dhau los ntawm ntau tiam neeg ntawm cov kab mob ua ntej raug ntxias (xws li los ntawm kev ntxhov siab) rau hauv lytic phages thiab tua cov kab mob [150], ib qho kev hloov pauv hauv cov kab mob microbiome thaum lub sij hawm sepsis tuaj yeem ua rau muaj kev hloov pauv hauv Sirota (virome). Tseeb tiag, fecal Sirota los ntawm cov nas septic qhia tau tias muaj kev hloov pauv ntawm ntau pawg ntawm cov kab mob bacteriophages, suav nrog Myoviridae (hauv sham nas) thiab Podoviridae (hauv septic nas), uas yog cov khoom ntawm ntau phage cocktails siv hauv lwm cov kev tshawb fawb [15]. Qhov kev soj ntsuam hais tias cov kab mob sib cais los ntawm cov quav ntawm tus nas septic tuaj yeem ua rau mob sepsis hauv lwm tus nas [15] ua rau muaj qhov tshwm sim ntawm cov kab mob kev nyuab siab thaum lub sij hawm sepsis activates lytic phages uas yuav muaj peev xwm tswj tau qee cov kab mob sepsis-induced pathogenic cov kab mob. Phages accumulating nyob rau hauv lub mucosal txheej yuav ua tau ib tug barrier rau kab mob ntxeem tau; Txawm li cas los xij, cov kab mob uas qhia txog phage-encoded proteins tuaj yeem ua rau muaj kev phom sij ntau ntxiv (epithelial ntxeem tau, adhesion, tshuaj tiv thaiv kab mob, phagocytosis blockage, thiab biofilm tsim) thiab kev thauj mus los ntawm phages los ntawm transcytosis ntawm phage particles thiab / lossis apical-basal thauj tuaj yeem xa cov phages rau hauv. kev ncig thiab txhim kho inflammatory teb [151,152]. Hmoov tsis zoo, kev tshawb fawb ntawm plab virota (los yog phageomes), tshwj xeeb tshaj yog nyob rau hauv sepsis, tsis tshua muaj.
Daim duab 2. Kev kho mob ntawm prebiotics, probiotics, thiab FMT nyob rau hauv cov nqe lus ntawm plab hnyuv permeability cuam tshuam Tag nrho cov tswv yim no txhim kho qhov sib npaug ntawm plab microbiota nrog ntau cov kab mob sib txawv uas muaj txiaj ntsig zoo rau tus tswv tsev los ntawm kev txo cov kab mob microbes, ntxiv dag zog rau lub plab barrier thiab induces. lub plab epithelial reconstruction. Daim duab yog tsim los ntawm BioRender.com
Adjunctive kev kho mob
Vim tias muaj kev sib raug zoo ntawm plab dysbiosis thiab sepsis hnyav, kev tswj hwm ntawm plab microbiome (thiab plab barriers) tuaj yeem tiv thaiv plab hnyuv sepsis lossis attenuate sepsis hnyav los ntawm kev ntxiv dag zog rau lub plab barrier, txo cov kab mob plab, txo cov ntsiab lus PAMP (LPS thiab BG) hauv plab thiab tshem tawm cov lus teb ncaj qha los tiv thaiv. Qhov normalization ntawm plab microbiota los ntawm ntau txoj hauv kev, suav nrog kev hloov fecal (kev tswj hwm kev noj qab haus huv microbiota), probiotics (cov kab mob muaj txiaj ntsig) (Daim duab 2), prebiotics (probiotic-txhim kho cov tshuaj), thiab synbiotics (probiotics nrog prebiotics), tau raug kuaj hauv sepsis. .
Fecal microbiota hloov pauv
Ntau qhov kev tshawb fawb tsiaj thiab cov ntaub ntawv xov xwm tau tshaj tawm lub peev xwm ntawm fecal microbiota hloov pauv (FMT) kom txo qis sepsis qhov hnyav, ib feem los ntawm kev kho cov kab mob butyrate-ua, lub plab barrier ntxiv dag zog rau lub cev, kev tiv thaiv kab mob hauv lub cev, kev hloov pauv hauv lub cev, thiab kev tshem tawm cov kab mob; Txawm li cas los xij, qee qhov kev tshawb fawb tau tshaj tawm cov kab mob tuag taus [153]. Qhov tseem ceeb, lub cev tiv thaiv kab mob yog ntau yam receptors ntawm T hlwb thiab B hlwb uas muaj ntau yam sib txawv kom paub txog cov kab mob sib txawv raws li ib feem ntawm lub cev tiv thaiv kab mob [154], thiab kev tiv thaiv innate, piv txwv li, macrophages, yog ib qho Tus tswv tsev tseem ceeb teb tawm tsam kab mob plab hnyuv [74].
Lub caij no, butyrate yog ib qho tseem ceeb luv luv-chain fatty acid uas yog categorized li enterocyte zog qhov chaw thiab ib qho tseem ceeb ntawm kev tiv thaiv kab mob thiab anti-malignancy [155]. Tom qab ntawd, FMT kev tswj hwm zoo li txhim kho cov txiaj ntsig ntawm kev tswj hwm kab mob hauv lub cev los ntawm kev txhim kho hauv lub cev thiab kev tiv thaiv kab mob ua ke nrog kev txhawb nqa enterocyte kev ncaj ncees uas yuav muaj txiaj ntsig zoo hauv sepsis [156]. Clostridium difficile zoo li yog thawj kab mob nrog FMT kev soj ntsuam cuam tshuam. C. difficile yog cais raws li kab mob Gram-positive kab mob ua rau kis kab mob colitis uas nquag tshwm sim tom qab siv tshuaj tua kab mob ntau dhau [157]. C. difficile ua rau muaj teeb meem ntawm kev kho tshuaj tua kab mob vim nws cov kab mob rov tshwm sim. Qhov zoo siab, kev siv FMT los ntawm cov tshuaj hauv qhov ncauj lossis FMT colonoscopy hauv cov neeg mob uas rov muaj C. difficile tau pom cov txiaj ntsig tau zoo (96.2% thiab 96.1% ntawm cov neeg mob tau kho tom qab 12-lub limtiam kev kho mob los ntawm qhov ncauj FMT thiab colonoscopy FMT, feem) [158]. Qhov cuam tshuam hloov tshiab ntawm FMT tam sim no koom nrog nws cov ntawv thov raws li kev kho mob qog noj ntshav. Qhov peev xwm no raws li kev kho mob tau pom thawj zaug hauv cov nas uas mob qog noj ntshav tab sis tsis muaj microbiome, vim tias cov tsiaj no tau pom cov lus teb sib txawv thaum kho nrog cov tshuaj tiv thaiv kab mob, suav nrog cisplatin, cyclophosphamide, thiab tiv thaiv kab mob cell tuag 1 protein (PD-1) immunotherapy [159,160]. Cov kev tshawb pom no kuj tau txais kev txhawb nqa los ntawm cov pov thawj tias Enterococcus faecalis tuaj yeem ncaj qha metabolize levodopa [161]. Yog li ntawd, kev siv plab microbiota ua ke nrog cov tshuaj tuaj yeem muaj txiaj ntsig zoo rau qhov sib npaug ntawm plab hnyuv microbes, yog li ib txhij txo qis cov kab mob plab thaum qee yam kev kho mob. Txawm li cas los xij, nyob rau nruab nrab -2019, US Food and Drug Administration (FDA) tau tshaj tawm tias FMT txoj kev kho yuav tsum tau siv nrog ceev faj, raws li cov ntaub ntawv ntawm kev tuag ntawm kev ncua-spectrum -lactamase (ESBL)-ua rau Escherichia coli kab mob. [162]. Raws li qhov tshwm sim, FDA tau tshaj tawm cov lus ceeb toom tias kev tshuaj xyuas qhov tob rau txhua tus kab mob tiv thaiv yuav tsum tau ua ua ntej FMT.
Probiotics
Nyob rau hauv sib piv rau tej yam tshwm sim loj tshwm sim ntawm FMT nyob rau hauv sepsis kev kho mob sepsis, cov kev phiv ntawm probiotics feem ntau yog tsawg, vim hais tias feem ntau probiotics yog anaerobes thiab anaerobic bacteremia tsis yog ib txwm mob hnyav thiab yog yooj yim rau kho piv nrog aerobic bacteriaemia [163]. Probiotics muaj PAMPs; Yog li, lub plab translocation ntawm probiotics lossis lawv cov khoom tuaj yeem ua rau lub cev tiv thaiv kab mob. Yog li ntawd, kev tswj hwm ntawm probiotics rau cov tib neeg uas muaj kev tiv thaiv kab mob los yog cov hnub nyoog hnyav, mob hnyav, lossis nrog cov plab hnyuv loj tuaj yeem ua rau cov kab mob bacteremia [164,165]. Hauv qee qhov xwm txheej, nrog rau cov probiotics uas tsim nyog, lub plab khoob yuav muaj txiaj ntsig zoo vim qee qhov muaj txiaj ntsig zoo los ntawm cov kab mob probiotics tuaj yeem thauj mus los ntawm lub plab puas tsuaj [54,55]. Probiotics potentiate colonization kuj los ntawm lawv cov dej num ntawm txo luminal pH, antimicrobial zog, thiab sib tw rau cov as-ham thiab adhesion nto [36,37]. Tseeb tiag, qee hom Lactobacillus thiab Bifidobacterium tsim qee cov exopolysaccharides nrog cov tshuaj tiv thaiv kab mob [166,167], thaum tseem txo cov kab mob los ntawm kev sib tw khoom noj khoom haus, quorum sensing antagonists, thiab tsim cov tshuaj uas cuam tshuam cov kab mob [168]. Ntau hom kab mob yog cov kev xaiv rau probiotics, tab sis qee cov kab mob yuav ua rau muaj kev phom sij ntau dua li lwm tus. Piv txwv li, enterococci tuaj yeem ua rau endocarditis hauv qee yam mob, thaum lactobacilli thiab Bifidobacterium kho tau yooj yim [169]. Probiotics kuj txhim khu plab hnyuv muaj nuj nqi los ntawm mucin ntau lawm thiab nruj hlws ris proteins. Tam sim no, probiotics tau txuas ntxiv mus rau lwm yam kev siv, suav nrog kev tiv thaiv ntawm daim tawv nqaij los ntawm ntau yam kab mob, xws li Staphylococcus, Corynebacterium, thiab Propionibacterium, tab sis qhov kev siv no tuaj yeem ua rau kev txhim kho ntawm daim tawv nqaij tiv thaiv kab mob, xws li rosacea [170]. Interestingly, hauv zos daim ntawv thov ntawm probiotics txhim kho daim tawv nqaij colonization los ntawm Cutibacterium acnes [171]. Tsis tas li ntawd, cov ntaub ntawv ntawm qhov ncauj ntawm probiotics, xws li Lactobacillus reuteri, tau pom muaj peev xwm txo qis perifollicular o los ntawm kev txhawb nqa lub plab-brain-skin (GBS) axis [172].
Prebiotics
Qhov laj thawj rau kev siv cov prebiotics hauv cov plab hnyuv plab yog qee yam khoom noj khoom haus tuaj yeem txhawb kev loj hlob ntawm qee yam kab mob plab uas cuam tshuam nrog kev noj qab haus huv rau tus tswv [173]. Prebiotics tsis yog tsuas yog cov khoom noj uas tsis yog digestible los ntawm tus tswv tsev uas txhawb cov kab mob fermenting nyob rau hauv txoj hnyuv [174] tab sis kuj yog cov as-ham degraded los ntawm lub plab hnyuv microbiota uas hloov cov microbiome txoj haujlwm thiab muaj pes tsawg leeg [175]. Ntau hom kev noj zaub mov muaj npe hu ua prebiotics nyob rau hauv cov categorizations, tshwj xeeb tshaj yog cov khoom lag luam muaj carbohydrate-based noj fibers (polymers ntawm monosaccharides), uas yog fermented los ntawm plab hnyuv microorganisms. Cov as-ham no tau zom los tsim ntau lub molecules, xws li SCFAs thiab peptidoglycan, uas cuam tshuam rau lub cev tsis muaj zog [176]. Prebiotics tuaj yeem txhim kho cov tshuaj insulin tsis kam thiab qabzib kam rau ua [177] thiab txo cov plab hnyuv, endotoxemia, thiab cytokines uas tej zaum yuav muaj txiaj ntsig zoo hauv sepsis. Raws li xws li, desaminotyrosine (DAT) tswj mucosal immunological homeostasis thiab thaiv kev ncaj ncees thiab txo cov mucosal o hauv DSS-induced endotoxemia thiab septic shock hauv nas [178]. Qee cov tshuaj prebiotics los ntawm Suav tshuaj ntsuab, Xuanbai Chengqi decoction (XBCQ), kuj txo qis kev mob ntsws ntsws hauv cov nas los ntawm kev txhim kho plab hnyuv ua haujlwm thiab txhawb kev ciaj sia [179,180]. Tsis tas li ntawd, Finger Millet arabinoxylan (FM-AX), uas tsis yog cov hmoov txhuv nplej siab polysaccharide uas tsim los ntawm cov nplej, txo qis endotoxemia hauv cov nas los ntawm kev txo qis ntawm cov rog rog uas ua rau lub plab [181]. Hauv tib neeg kev tshawb fawb, prebiotics txo qhov tshwm sim ntawm sepsis, kev tuag, thiab ntev nyob hauv tsev kho mob hauv cov me nyuam mos ntxov ntxov [182]. Thaum tus nqi npaj rau FMT thiab probiotics feem ntau yog siab nrog cov thev naus laus zis thev naus laus zis vim yog kev tswj hwm cov kab mob uas siv tau, kev npaj prebiotics zoo li tsis tshua kim nrog, tej zaum ntev dua lub txee. Txawm li cas los xij, prebiotics tsis tuaj yeem txhawb kev loj hlob ntawm cov kab mob uas tsis muaj nyob hauv plab, thiab cov khoom lag luam feem ntau yog kev sib xyaw ua ke ntawm prebiotics nrog probiotics. Vim tias cov txheej txheem pheej yig dua ntawm kev npaj, cov prebiotics, ib leeg lossis hauv kev sib xyaw ua ke, xaiv txhawb kev loj hlob ntawm cov kab mob uas muaj txiaj ntsig zoo uas feem ntau pom hauv tus tswv tsev hauv sepsis yog qhov nthuav. Muaj kev tshawb fawb ntxiv.
cistanche cog-nce kev tiv thaiv kab mob
Cov lus xaus
Lub plab to thiab kev hloov pauv hauv plab hnyuv microbiome hauv sepsis yog qhov tshwm sim ntawm plab hnyuv tiv thaiv kab mob tshwm sim los ntawm plab hnyuv hypoperfusion, lub cev tiv thaiv kab mob apoptosis, thiab enteric neuro-humoral-immunity teb. Kev nce ntxiv ntawm cov kab mob hauv cov kab mob microbiome cuam tshuam nrog lub plab zom mov tuaj yeem ua rau kev hloov pauv ntawm cov kab mob microbial thiab txawm tias cov kab mob ua tau zoo, thaum kawg ua rau cov kab mob sepsis. Txawm hais tias muaj ntau qhov kev tshuaj xyuas yav dhau los ntawm lub plab microbiota hauv sepsis [183–186], kev sau cov ntaub ntawv ntawm plab mycobiome (fungiome) thiab microbiome feem ntau yog txwv rau cov mob uas tsis yog mob sepsis [187–190] thiab kev tshuaj xyuas ntawm plab microbiome ua ke nrog rau cov pa tawm. plab hauv sepsis tseem tsawg dua. Ntawm no, kev sib raug zoo ntawm plab microbiota (cov kab mob, fungi, thiab kab mob) thiab sepsis hnyav kuj qhia tau hais tias kev txo qis ntawm cov plab hnyuv thiab plab dysbiosis tej zaum yuav yog lub hom phiaj ntawm kev kho mob yav tom ntej. Ntxiv mus, lub luag hauj lwm ntawm virome, mycobiome, nrog rau cov tshiab metagenomics ntawm microbial identification yuav tsum yog nyob rau hauv lub pipeline ntawm yav tom ntej kev tshawb fawb cheeb tsam thiab yog urgently xav tau teb.
Cov ntaub ntawv
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