Crosstalk Ntawm Gut Microbiota Thiab Kev Tiv Thaiv Tus Kheej: Kev cuam tshuam rau Kev Mob thiab Kev Kho Mob (1)
Oct 23, 2023
Abstract: Lub plab microbes thiab lawv cov metabolites nquag koom nrog hauv kev txhim kho thiab kev tswj hwm kev tiv thaiv tus tswv, uas tuaj yeem cuam tshuam cov kab mob. Ntawm no, peb tshuaj xyuas cov kev tshawb fawb tshiab tshaj plaws hauv plab microbiota-cov kab mob tiv thaiv kab mob. Peb sib tham txog kev nthuav dav li cas lub plab microbiota yog qhov taw qhia rau kev txhim kho lub cev tsis muaj zog raws li qhia los ntawm cov xwm txheej tshiab uas tsis tau pom dua, xws li niam txiv imprinting, in-utero plab hnyuv metabolome, thiab weaning cov tshuaj tiv thaiv. Peb piav qhia txog yuav ua li cas lub plab microbiota zoo li ob qho tib si hauv lub cev thiab kev tiv thaiv kab mob nrog rau qhov tseem ceeb ntawm cov metabolite's short-chain fatty acids thiab cov kua tsib acids. Peb kuj qhia meej txog qhov kev cuam tshuam ntawm microbiota-immune axis ua rau cov kab mob tiv thaiv kab mob, xws li kab mob hauv plab, kab mob plab, kab mob plawv (xws li, kab mob plawv, ntshav qab zib, thiab kub siab), autoimmunity (xws li, mob caj dab rheumatoid), hypersensitivity (piv txwv li, mob hawb pob thiab ua xua), kev puas siab puas ntsws (xws li, ntxhov siab vim), thiab mob qog noj ntshav (xws li mob plab thiab mob siab). Peb ntxiv rau lub luag haujlwm ntawm kev hloov pauv fecal microbiota, probiotics, prebiotics, thiab kev noj haus polyphenols hauv kev kho lub plab microbiota thiab lawv cov peev xwm kho tau. Txuas ntxiv mus, peb tshuaj xyuas seb lub plab microbiota hloov kho kev tiv thaiv kab mob li cas, suav nrog cov tshuaj tiv thaiv kab mob, JAK inhibitors, thiab tshuaj tiv thaiv TNF. Peb kawg hais txog cov teeb meem tam sim no hauv metagenomics, qauv tsis muaj kab mob, thiab microbiota recapitulation kom ua tiav qhov kev nkag siab ntawm lub plab microbiota li cas tswj kev tiv thaiv kab mob. Ua ke, qhov kev tshuaj xyuas no qhia txog kev txhim kho kev siv tshuaj tiv thaiv kab mob los ntawm kev pom ntawm microbiome-targeted interventions.
cistanche tubulosa- txhim kho lub cev tiv thaiv kab mob
Ntsiab lus: plab microbiota dysbiosis; innate tiv thaiv kab mob; adaptive tiv thaiv kab mob; kab mob; mob qog noj ntshav; inflammatory plab hnyuv kab mob; fecal microbiota hloov pauv
cistanche tubulosa- txhim kho lub cev tiv thaiv kab mob
Nyem qhov no mus saib Cistanche Enhance Immunity khoom
【Nug ntxiv】 Email: cindy.xue@wecistanche.com / Whats App: 0086 18599088692 / Wechat: 18599088692
1. Taw qhia
Tsis muaj txiv neej yog ib kob, hais tias John Donne, los piav txog kev sib raug zoo ntawm tib neeg thiab zej zog [1]. Txawm li cas los xij, qhov no kuj muaj tseeb thaum piav txog tib neeg cov metabolism. Txij li thaum yug los, tib neeg, zoo li tag nrho lwm yam tsiaj, raug colonized los ntawm microbes, tshwj xeeb tshaj yog nyob rau ntawm daim tawv nqaij thiab mucosal nto, xws li lub plab zom mov (GIT). GIT harbors ib qho kev sau ntau ntawm cov kab mob hu ua lub plab microbiota. Nws yog ib qho kev sib npaug ntawm ntau tshaj 5000 hom kab mob hauv cov kab mob (xws li, 99% ntawm cov hnyuv microbiota yog tsim los ntawm Firmicutes, Bacteroidetes, Proteobacteria, thiab Actinobacteria), fungi (xws li, Candida), kab mob (xws li, bacteriophages), thiab kab mob cab. (eg, flagellates) [2–8]. Lub plab microbiota ua zoo li 'superorganism' hauv tib neeg lub tswv yim thiab pab hauv kev sib xyaw ntawm cov zaub mov, tsim cov metabolites uas txhawb nqa tus tswv tsev, tiv thaiv tus tswv ntawm kev kis kab mob, tswj kev ua haujlwm thiab morphology ntawm plab hnyuv epithelial hlwb, thiab tswj kev tiv thaiv tus tswv tsev [4, 8–12] ib. Raws li kev noj qab haus huv, lub plab microbiota yog nyob rau hauv lub xeev sib npaug ntawm 'eubiosis'. Txawm li cas los xij, thaum muaj kab mob, lub plab microbiota nkag mus rau hauv lub xeev tsis sib haum xeeb ntawm dysbiosis nyob rau hauv uas muaj ib qho kev tawg ntawm cov kab mob kis tau zoo txo qis hauv cov txiaj ntsig zoo, lossis ob qho tib si. Kev zoo nkauj ntawm tus tswv tsev-microbiota kev sib raug zoo nyob rau hauv qhov tseeb tias microbes zoo li txhua yam ntawm tib neeg cov metabolism. Xws li, ntxiv rau kev zom zaub mov thiab tawv nqaij, lub plab microbiota muaj peev xwm cuam tshuam rau cov kab mob pathogenesis, xws li rog thiab mob hawb pob, thiab kev puas siab puas ntsws, xws li Parkinson's disease [13,14]. Lub plab microbiota crosstalk nrog tus tswv tsev tiv thaiv kab mob yog ib qho ntawm cov yam ntxwv tseem ceeb ntawm kev ruaj ntseg ntawm lub cev thiab lub tshuab rau kab mob etiology. Muaj ob ceg ntawm lub cev tiv thaiv kab mob, piv txwv li, innate thiab adaptive, uas ua haujlwm ua ke los tiv thaiv lub cev los ntawm kev hem sab nraud thiab sab hauv. Lub cev tiv thaiv kab mob hauv lub cev yog 'thawj kab ntawm kev tiv thaiv' thiab muab cov lus teb ceev ceev tsis yog tshwj xeeb raws li kev tiv thaiv kab mob. Innate kev tiv thaiv muaj xws li granulocytes, natural killer cells, dendritic cells, thiab macrophages uas engulf cov kab mob thiab secrete cytokines thiab chemokines. Ntxiv nrog rau kev nrhiav neeg ua haujlwm ntawm lub cev tiv thaiv kab mob ntau dua, cytokines nyiam lymphocytes, piv txwv li, B hlwb, uas tsim cov tshuaj tiv thaiv tshwj xeeb rau cov kab mob tshwj xeeb, thiab T hlwb (feem ntau categorized rau hauv pab T hlwb, cytotoxic T hlwb, thiab tswj T hlwb ( Treg hlwb)), ob qho tib si uas tsim lub hauv paus ntawm kev tiv thaiv kab mob [15,16]. Ob txhais caj npab ntawm lub cev tiv thaiv kab mob yog nruj tswj hwm kom tsis txhob muaj kev ua kom dhau los lossis ua rau qaug zog, uas lub plab microbiota yog qhov tseem ceeb (cov ntsiab lus hauv Graphical Abstract). Hauv qhov kev tshuaj xyuas no, peb muab cov lus piav qhia tob thiab sib tham txog yuav ua li cas lub plab microbiota tag nrho, ntxiv rau cov kab mob tshwj xeeb thiab cov metabolites los ntawm microbial, tswj kev tiv thaiv kab mob. Peb tham ntxiv txog yuav ua li cas lub plab microbiota - lub cev tiv thaiv kab mob tsis zoo nyob rau hauv cov kab mob uas muaj kab mob ntev heev thiab yuav ua li cas hloov kho lub plab microbiota tuaj yeem yog kev kho lossis ua tau rau lwm yam kev kho mob tam sim no.
2. Lub luag haujlwm ntawm Gut Microbiota thiab lawv cov metabolite hauv Neonatal Immune System Development
Thawj microbial colonization nyob rau hauv ib tug neonate nyob ntawm hom kev xa (C-section vs. vaginal delivery) thiab pub mis (formula vs. niam mis) [17–19]. Piv txwv li, kev pub mis mis pom tau tias txo qis qhov sib txawv ntawm lub plab microbiota thiab nthuav cov kab mob pathogenic, xws li Enterobacteriaceae thiab Enterococcaceae; Cov plab hnyuv microbiota dysbiosis no tau ua rau muaj ntau dua mucosa inflammatory kev ua thiab ua rau cov kab mob phem zuj zus hauv tus qauv necrotizing enterocolitis [20]. Ntxiv mus, muaj peev xwm ua tau rau C-section los cuam tshuam niam-rau-neonate kis tau tus mob tshwj xeeb microbial hom (xws li, LPS-expressing bacteria) tau tshaj tawm [21]. Txawm li cas los xij, lub cev tsis muaj zog tiv thaiv kab mob tuaj yeem ua rau muaj kev loj hlob hauv lub tsev menyuam vim tias cov kab mob feem ntau tshwm sim hauv niam txiv lub plab thiab qhov ncauj, xws li Firmicutes, Actinobacteria, thiab Proteobacteria, muaj nyob rau hauv placenta, umbilical qaum, thiab amniotic kua [22,23. ]. Thaum lub microbiome nyob rau hauv-utero tseem tab tom tshawb nrhiav, ib tsab xov xwm 2020 los ntawm Rackaityte li al. tawm tswv yim tias kab mob colonization yuav txwv nyob rau hauv tib neeg txoj hnyuv nyob rau hauv utero [24]. Tsis tas li ntawd, cov pov thawj tsis ntev los no rau hauv-utero plab hnyuv metabolome tau piav qhia thiab pom tias muaj cov amino acids (piv txwv li, tryptophan), cov vitamins (xws li, riboflavin), thiab, tshwj xeeb tshaj yog, plab-microbiota-derived bile acids [25]. Lub tswv yim ntawm kev nyiam huv tau hais tias kev kis mus rau ntau ntau ntawm microbes thaum ntxov hauv lub neej yog qhov tseem ceeb los txhim kho lub cev tiv thaiv kab mob [26]. Thaum lub sij hawm intra-uterine txoj kev loj hlob, lub fetal innate lub cev tiv thaiv kab mob yog suppressed los ntawm Foxp 3+ CD4+ Treg hlwb los tiv thaiv kev tiv thaiv kab mob tiv thaiv leej niam antigens [12]. Thaum thiab tom qab yug me nyuam, antigens los ntawm commensals tau lees paub los ntawm ntau tus qauv lees paub receptors (PRRs), xws li Tus Xov Tooj Zoo li receptors (TLRs), ntawm plab hnyuv epithelia, ua rau muaj cov tshuaj tua kab mob tsawg dua thiab tsim kom muaj kev tiv thaiv kab mob [27]. Nrog rau cov no, Paneth hlwb tsim cov tshuaj tua kab mob peptides, xws li phospholipase -2, lysozyme, thiab defensins, tab sis cov molecules no tsis ua tawm tsam commensals thiab tiv thaiv lub plab neonatal los ntawm cov kab mob kis tau zoo [22,28]. Bifidobacteria spp. yog ib qho ntawm cov ntsiab lus tseem ceeb uas cuam tshuam rau kev tiv thaiv menyuam mos, xws li T cell maturation [29]. Qhov tsis muaj Bifidobacteria ua rau cov neeg ua kua mis oligosaccharide depletion thiab tau txuam nrog ntau dua Th2/Th17 kev tiv thaiv kab mob [30]. Nws yog qhov tsim nyog tias kev pub mis mis yog txuam nrog tsawg Bifidobacteria abundance, tab sis cov nyhuv yog ib ntus [31]. Tom qab lactation, cov menyuam yaus tau txais cov txheej txheem tshiab hu ua 'weaning reaction', uas yog kev hloov pauv hauv lub plab microbiota uas tshwm sim thaum cov xeeb ntxwv hloov ntawm cov kua mis mus rau cov khoom noj [32]. Weaning cov tshuaj tiv thaiv tau pom los ua kom cov kab mob thiab cov khoom noj khoom haus metabolites, xws li luv-chain fatty acids (SCFA) thiab retinoic acid [32]. Inhibition ntawm weaning ua rau pathological imprinting rau muaj kev pheej hmoo ntawm kev tsis haum o thiab colitis [32]. Qhov no sib tw rau lwm cov lus ceeb toom tias qhov tsis tuaj yeem tshwm sim thaum ntxov ntawm microbiota tuaj yeem ua rau immunoglobin E (IgE) ntau dhau thiab ua rau muaj kev cuam tshuam rau ntau yam antigens, uas ua rau muaj mob xws li mob hawb pob thiab mob plab hnyuv [33–35]. Zuag qhia tag nrho, kev loj hlob ntawm lub cev tiv thaiv kab mob thaum ntxov yog tswj hwm los ntawm lub plab microbiota thiab tuaj yeem muaj kev cuam tshuam ntev rau kev kis kab mob.
cistanche tubulosa- txhim kho lub cev tiv thaiv kab mob
3. Kev sib cuam tshuam ntawm Gut Microbiota thiab Host Innate Immune System
Kev sib cuam tshuam ntawm plab microbiota thiab tus tswv tsev mucosal tiv thaiv kab mob yog qhov tseem ceeb hauv kev tswj hwm kev noj qab haus huv ntawm tus tswv tsev vim nws yog thawj kab ntawm kev tiv thaiv tawm tsam cov kab mob hauv plab (cov ntsiab lus hauv Graphical Abstract). Lub mucosal nto yog compartmentalized nrog lub cev tiv thaiv kab mob, nrog rau ib tug tuab mucus txheej, kaw ntom nti proteins, thiab antimicrobial proteins. Cov kab mob hauv plab hauv lub cev tiv thaiv kab mob txhim kho kev ua siab ntev rau cov kab mob commensal los ntawm kev txheeb xyuas cov kab mob nkag mus thiab tiv thaiv lawv txoj hauv kev los ntawm txoj hnyuv lumen mus rau kev ncig [36]. Tom qab trespassing los ntawm lub epithelial barrier, invasive kab mob thiab pathogen-txuas molecular qauv (PAMPs, piv txwv li, lipopolysaccharides / LPS) tuaj yeem txhawb kev tso tawm ntawm mucin los ntawm goblet hlwb thiab induce sai reconstitution ntawm lub puab mucous txheej [37]. PAMPs tseem tuaj yeem ua rau muaj kev tiv thaiv kab mob hauv lub cev los ntawm kev ua kom TLRs ntawm neutrophils thiab macrophages [38]. Cov kab mob Commensal kuj tseem tuaj yeem ua rau cov hlwb dendritic (DCs) ntawm lawv qhov kev nthuav qhia antigen, uas, dhau los, tuaj yeem qhib TLRs los cob qhia cov kab mob hauv lub cev kom paub txog cov kab mob thiab cov kab mob commensal [39]. Ntxiv mus, invading microbes yog phagocytosed thiab eradicated los ntawm mucosal innate lub cev tiv thaiv kab mob, xws li DCs thiab macrophages nyob rau hauv noj qab haus huv tej yam kev mob [40]. Ntawm qhov kev ceeb toom, tshwj xeeb DC subsets tuaj yeem cuam tshuam cov kab mob uas muaj kab mob hauv lamina propria ntawm lub xeev khov kho [41]. Nws tseem tsis ntev los no tau pom tias qhov kev loj hlob ntawm cov neeg ua ntej ntawm hom 1 cov pa DCs yog kho los ntawm plab-microbiota-induced qog necrosis factor (TNF) secretion los ntawm monocytes thiab macrophages [42]. Ntxiv rau cov macrophages, neutrophils, thiab DCs, muaj cov kab mob tshwj xeeb ntxiv, xws li goblet hlwb thiab Paneth hlwb, uas tso tawm ntau yam tshuaj tua kab mob, xws li mucins, defensins, lysozyme, secretory phospholipase A2, thiab cathelicidins; lawv ua cov khoom siv tiv thaiv kab mob kom txhawb nqa lub plab hauv lub cev tiv thaiv kab mob [43,44]. Innate lymphoid cells (ILCs) yog lwm ceg ntawm lub cev tiv thaiv kab mob hauv lub cev uas feem ntau tsis yog cytotoxic thiab secrete ntau yam effector cytokines [45]. Ua ke, ntau lub cev tiv thaiv kab mob hauv lub cev muaj lub plab microbiota homeostasis. Hauv kev kho mob, kev hloov pauv ntawm enteric microenvironment txhawb txoj kev loj hlob ntawm cov kab mob thiab txo qis cov kab mob commensal, piv txwv li, plab microbiota dysbiosis [46], uas ua rau cov lus teb tsis txaus ntseeg (cov ntsiab lus hauv Graphical Abstract). Nyob rau hauv ib puag ncig pathologic, neutrophils tau koom nrog ntau dhau ntawm qhov chaw mob lossis kis kab mob thiab tuaj yeem ua rau muaj kev puas tsuaj rau mucosal los ntawm kev ua kom cov cytokine secretion, matrix metalloprotease ntau lawm, thiab pathologic immune cell activation [43,47]. Neutrophils feem ntau khaws cia rau hauv lub xeev quiescent los tiv thaiv kev cuam tshuam ntawm plab microbial ecology, uas yog kho los ntawm adapter protein downstream ntawm kinase 3 [48]. Interestingly, qhov induction ntawm neutrophil extracellular ntxiab (NETs) coj mus rau pathogen clearance thiab txo o [49]. Cov tshuaj tua kab mob hauv plab microbiota dysbiosis kuj tau pom los ua rau NET tsim, tab sis qhov no tau cuam tshuam nrog kev mob hnyav dua [50], hais tias yuav tsum tau tshawb xyuas ntxiv los txiav txim siab lub luag haujlwm ntawm txoj hnyuv NETs. Zuag qhia tag nrho, qhov pib tsim nyog lossis qhov sib npaug ntawm lub cev tiv thaiv kab mob hauv lub cev thiab lub plab microbiota yog qhov tseem ceeb los txhawb nqa homeostasis thiab tiv thaiv cov txiaj ntsig ntawm pathophysiologic.
4. Kev sib cuam tshuam ntawm Gut Microbiota thiab Adaptive Immune System
Lub cev tiv thaiv kab mob hauv lub plab mucosa feem ntau yog intraepithelial lymphocytes (IELs) thiab lamina propria lymphocytes (LPLs) [51]. Ntawm cov IELs, δ T hlwb yog ib qho sib txawv ntawm T hlwb vim lawv qhia txog Helios transcription factor [52]. δ T lymphocytes inhibit qhov mucosal tshaj tawm ntawm cov kab mob los ntawm kev zais cov cytokines pro-inflammatory thiab antimicrobial proteins [53,54]. Piv txwv li, δ T hlwb txhawb CD4+ T cell teb, xws li mucosal tso tawm ntawm IL-22 thiab calprotectin [55]. Ntau hom kab mob hauv plab thiab lawv cov metabolites tau sau tseg los txhawb kev nthuav dav ntawm δ T hlwb, suav nrog Desulfovibrio-derived phosphatidylethanolamine thiab phosphatidylcholine [56]. Cov kev tshawb fawb tau pom tias thaum intraepithelial δ T hlwb tsis txaus, muaj cov kab mob ntau dua thiab nthuav tawm cov kab mob sib kis [57]. Qhov no tau txais kev txhawb nqa los ntawm kev txo qis δ T hlwb hauv cov neeg mob septic septic [58,59] thiab txo cov kab mob δ T hauv cov neeg mob plab inflammatory [60]. Kev sib cuam tshuam ntawm plab microbiota thiab lub cev tiv thaiv kab mob tiv thaiv kab mob kis tau thiab kis kab mob (luam tawm hauv Graphical Abstract). Qhov no tau txais kev txhawb nqa los ntawm kev tshawb pom tias lub plab yoog lub cev tiv thaiv kab mob yog txwv tsis pub cov nas tsis muaj kab mob, thiab kev qhia txog cov kab mob commensal tuaj yeem txhawb kev loj hlob ntawm mucosal lymphocytes, xws li CD4+ T hlwb thiab cytotoxic CD{{16 }} T cells [61]. Ob theem thawj thiab theem nrab ntawm cytotoxic CD8+ T cell tiv thaiv yog nyob ntawm CD4+ T hlwb, uas yuav tsum tau priming los ntawm cov kws tshaj lij antigen-presenting cells thiab tau nthuav dav los ntawm CD4+ T cell signaling [ 62] ib. CD8+ T hlwb tshem tawm cov kab mob hauv lub cev (xws li Salmonella), feem ntau yog pab los ntawm DC-mediated antigen nthuav qhia [63]. Salmonella enterica serovar Typhi tuaj yeem txhawb CD8+ T hlwb ntawm kev hloov pauv hloov pauv, piv txwv li, histone methylation thiab acetylation [64]. Cov ntaub so ntswg-neeg nyob nco CD8+ T hlwb yog qhov tseem ceeb los tiv thaiv cov kab mob rov qab, thiab qhov no tuaj yeem kawm los ntawm Transient Microbiota Depletion-boosted Immunization qauv, uas txwv tsis pub microbiota-mediated colonization resistance [65] ib ntus. Ntawm qhov tod tes, B hlwb tuaj yeem ua rau cov kab mob phagocytose, xws li Salmonella, thiab rov ua lub cim xeeb CD8+ T hlwb, ntawm kev nthuav qhia [66]. T helper 17 hlwb (Th17) kuj tseem muaj lub luag haujlwm sib txawv hauv ob qho tib si kev tiv thaiv tus tswv thiab cov lus teb hauv inflammatory. Nws zoo nkaus li tias feem ntau Th17 cov lus teb yog cov kab mob pathological, qhov twg ib qho kev tshawb pom tshiab yog cov kab mob zoo li plab hnyuv Th17 txhawb cov kab mob pathogenic effector T hlwb hauv cov kab mob hauv plab hnyuv ntxiv [67]. Interestingly, Th17 hlwb txhawb los ntawm segmented filamentous kab mob (SFB) yog non-inflammatory, whereas Th17 hlwb induced los ntawm Citrobacter spp. Yuav ua li cas yog pro-inflammatory [68] Cov kev tshawb fawb tau pom tias Th17 hlwb tsis nyob hauv cov nas tsis muaj kab mob thiab raug ntxias los ntawm cov kab mob tshwj xeeb, xws li SFB [69] thiab lwm cov kab mob commensal [70]. SFB-mediated IL-17 stimulation tau pom tias tau coj los ntawm cytokine (piv txwv li, IL-6) cov cim [71]. Lub plab microbiota kuj tuaj yeem kho cov lus teb Th17. Ib txoj kev tshawb nrhiav pom tias microbiome-dependent Th17 o yog tswj los ntawm 2,6-sialyl ligands, qhov twg 2,6-sialyltransferase deficiency induced mucosal Th17 teb [72]. Pathological Th17 hlwb kuj tuaj yeem txhawb nqa los ntawm Actinobacterium Eggerthella lenta los ntawm kev pab ntawm lub plawv glycoside reductase 2 enzyme [73] thiab Fusobacterium nucleatum ntawm cov saw luv fatty acid, butyrate [74]. Regulatory T hlwb (Treg) yog lwm lub cev tiv thaiv kab mob uas muab kev tiv thaiv kab mob hauv GIT. Thaum ntxov nyob rau hauv lub neej, ntuj Treg hlwb raug tsim nyob rau hauv lub thymus los ntawm ib tug autoimmune regulator rau nws tus kheej kam rau siab [75,76], thiab ces raug rau noj thiab microbiota teeb nyob rau hauv lub suab peripheral los yog inducible Treg ntau lawm [32,77–79]. Lub plab microbiota tuaj yeem tsim cov hlwb Treg los ntawm ntau lub tshuab. Piv txwv li, ILCs tuaj yeem xaiv microbiota-specific ROR t + Treg hlwb thiab tiv thaiv kev nthuav dav ntawm Th17 hlwb kom muaj kev tiv thaiv kab mob hauv cov hnyuv [80]. Helicobacter spp. [81] thiab Akkermansia muciniphila (A. muciniphila) [82] kuj tuaj yeem ua rau ROR t + Treg cell-mediated immune teb. Piv txwv li, txo qis ntawm lub plab-microbiota-derived metabolite propionate (a luv-chain fatty acid) tuaj yeem ua rau muaj kev tsis txaus ntseeg hauv Th17 / Treg cell sib txawv [83,84]. Lub plab microbiota kuj tseem ua lub luag haujlwm tseem ceeb hauv kev tswj hwm kev tsim cov secretory immunoglobulin A (IgA), uas yog tsom rau cov kab mob enteric commensals thiab cov kab mob antigens [85, 86]. Secretory IgA tuaj yeem tsim los ntawm T cell-dependent lossis T cell-ywj siab txoj hauv kev; T cell-dependent IgA ntau lawm yog qhov tseem ceeb hauv kev tsim cov plab hnyuv microbiota homeostasis [87]. Thaum ntxov hauv lub neej, IgA plasma hlwb muaj reactivity rau commensal microbiota, uas ua rau muaj kev sib npaug microbiome [88]. Cov ntaub ntawv pov thawj ntxiv hais txog kev luam tawm antigenic uas yog qhov tseem ceeb rau cov tshuaj tiv thaiv kab mob tom qab hauv lub neej [88,89]. Qhov no suav nrog IgA tso rau hauv cov kua mis, qhov uas niam hloov ntawm IgA yog qhov tseem ceeb rau kev tiv thaiv kab mob hauv cov xeeb ntxwv [90]. Thaum IgA tsis txaus, raws li qhia hauv nas, plab commensals tau yooj yim hla lub lamina propria, ua rau enteric kab mob translocation [91].
cistanche ntxiv cov txiaj ntsig-nce kev tiv thaiv
5. Crosstalk ntawm Microbial Metabolite thiab Immune Regulation
5.1. Short-Chain Fatty Acids
Lub plab microbiota muaj lub peev xwm loj hauv metabolic los hloov cov khoom noj khoom haus thiab cov khoom noj (lipids, carbohydrates, thiab proteins) rau hauv cov metabolites sib txawv uas tej zaum yuav muaj txiaj ntsig zoo lossis txaus ntshai rau tus tswv. Cov kab mob metabolites, xws li cov saw luv fatty acids (SCFAs), cov kua tsib theem nrab, lactic acid, thiab bacteriocins, muaj cov tshuaj tua kab mob uas tiv thaiv cov kab mob pathogenic [92,93]. SCFAs yog tsim los ntawm fermentation ntawm indigestible carbohydrates los ntawm ib co commensals, xws li Faecalibacterium prausnitzii, Roseburia intestinalis, thiab Anaerostipes butyraticus [94]. SCFAs tswj cov hnyuv homeostasis hauv cov hnyuv ib txwm los ntawm kev koom tes hauv kev kho cov hnyuv los ntawm cov cellular proliferation thiab sib txawv (Daim duab 1A). Acetate, feem ntau tsim los ntawm Bifidobacteria spp., tswj lub plab-- plab-epithelial barrier muaj nuj nqi thiab tswj cov hnyuv o los ntawm activating G-protein receptor (GPR) 43 [95]. Los ntawm GPR43 signaling, acetate txhawb microbiome-reactive IgA ntau lawm [96]. Qhov no cuam tshuam rau acetate yog ib qho ntawm cov plab hnyuv microbial metabolites kom nce colonic IgA ntau lawm thiab IgA txheej ntawm cov kab mob xws li Enterobacterales [97]. Acetate induction ntawm IgA yog qhov tseem ceeb los txhawb nqa plab microbiota hauv homeostasis. Hauv cov kab mob pathophysiologic, acetate thiab propionate, ib leeg lossis ua ke, tuaj yeem txo qhov mob los ntawm kev txo Th1 / Th17 thiab nce Treg qib [98]. Ib yam li ntawd, acetate supplementation rau cov dams nrog preeclampsia tuaj yeem rov qab los ntawm thymic Treg cell tso zis [99], thiab acetate pub rau cov nas uas tsis rog rog tuaj yeem txo qis autoreactive T hlwb [100]. Acetate kuj tau pom los txhawb T cell sib txawv rau hauv ob qho tib si effector thiab Treg hlwb, uas txo cov kab mob Citrobacter [101]. Butyrate ua feem ntau hauv plab hnyuv homeostasis ua lub zog tseem ceeb rau colonocytes [95] thiab txhawb kev tso tawm ntawm mucin los tswj lub plab barrier homeostasis (Daim duab 1A) [102]. Ntxiv nrog rau mucin, butyrate tuaj yeem txhawb nqa lub epithelial barrier los ntawm IL-10R -dependent repression ntawm claudin-2 [103]. Hauv kev tswj hwm lub cev tiv thaiv kab mob, butyrate tuaj yeem txhawb kev sib txawv ntawm monocyte-rau-macrophage los ntawm inhibiting histone deacetylase 3 (HDAC3) [104] thiab ua kom cov lus qhia ntawm IFN- thiab granzyme B hauv CD8+ T cells [105]. Ntxiv mus, butyrate tuaj yeem ua rau IL-22 tso tawm los ntawm T hlwb los ntawm kev txhawb nqa aryl hydrocarbon receptor (AhR) thiab hypoxia-inducible factor 1 qhia [106]. Zoo ib yam li acetate, butyrate tuaj yeem hloov kho lub cev tiv thaiv kab mob los ntawm kev ua kom GPR43 thiab ua kom muaj kev sib txawv ntawm Foxp3+ CD4+ Treg cells [100,107]. Butyrate tseem tuaj yeem txhawb kev tsim cov Treg inducible los ntawm kev ua kom cov roj acid oxidation nrawm [108] thiab inhibiting HDAC [109,110]. Piv txwv li, HDAC inhibitory cuam tshuam ntawm butyrate thiab propionate ntawm cov koob tshuaj siab txo qis hauv chav kawm-hloov DNA recombination hauv B hlwb, ua rau muaj kev puas tsuaj ntawm txoj hnyuv thiab lub cev T-dependent thiab T- ywj pheej cov tshuaj tiv thaiv kab mob [111]. Qhov no tuaj yeem piav qhia qhov kev tshawb pom los ntawm lwm daim ntawv tshaj tawm txog kev sib cuam tshuam ntawm cov qib IgA siab thiab qis SCFA qib uas cuam tshuam nrog kev tiv thaiv kab mob zoo dua [112]. Nco ntsoov, sib piv rau butyrate, propionate txo IL-17 thiab IL{55}} ntau lawm los ntawm plab hnyuv δ T cells [113]. Zuag qhia tag nrho, cov txheej txheem tseem ceeb uas SCFAs tswj hwm lub cev tiv thaiv kab mob hauv txoj hnyuv muaj xws li HDAC inhibition, GPR signaling, inhibiting pro-inflammatory cytokine secretion, thiab txhawb IgA ntau lawm (Daim duab 1A).
Daim duab 1. Muaj peev xwm ua tau ntawm cov saw hlau luv fatty acids thiab cov kua tsib acids muaj txiaj ntsig zoo rau lub cev tiv thaiv kab mob hauv IBD. (A) Short-chain fatty acids (SCFAs) yog fermented byproducts ntawm kev noj haus fiber ntau.
6. Kev cuam tshuam ntawm Environmental Microbiome Perturbation ntawm lub cev tiv thaiv kab mob
6.1. Antibiotic-Induced Microbiome Disturbances
Cov tshuaj tua kab mob tau txhim kho tib neeg lub peev xwm tiv thaiv kab mob. Txawm li cas los xij, qhov cuam tshuam ntawm cov tshuaj tua kab mob ntawm microbiome tsis tau txiav txim siab txog thaum tsis ntev los no. Cov kab mob hauv plab microbiota thiab lub cev tsis muaj zog tuaj yeem raug cuam tshuam rau niam txiv txoj haujlwm thaum lub pas dej microbiota raug tshuaj tua kab mob; Raws li qhov tshwm sim, cov xeeb ntxwv muaj kev pheej hmoo ntau ntxiv rau kev tsim cov kab mob, nrog rau cov kab mob plab hnyuv thiab cov kab mob autoimmune, thiab hypersensitivity, xws li mob hawb pob [128–134]. Ib yam li ntawd, kev kho tshuaj tua kab mob ncaj qha rau cov menyuam mos, tshwj xeeb tshaj yog cov menyuam mos yug ntxov, hloov lawv cov microbial muaj pes tsawg leeg thiab ua rau muaj kev cuam tshuam rau ntau yam kab mob, xws li necrotizing enterocolitis (NEC) [135–137]. Nws yog ib qho tseem ceeb uas fecal microbiota hloov los ntawm NEC cov neeg mob mus rau cov nas tsis muaj kab mob tau pom tias muaj kev txo qis hauv butyrate thiab Treg qib [138]. Kev siv tshuaj tua kab mob tsis tu ncua rau cov menyuam mos kuj tuaj yeem ua rau microbiota-dependent suppression ntawm hom 3 ILCs, uas ua rau cov kab mob lig pib tshwm sim [139]. Cov tshuaj tua kab mob tuaj yeem muaj ntau qhov cuam tshuam ncaj qha thiab tsis ncaj rau tib neeg kev noj qab haus huv, xws li kev txhim kho cov tshuaj tiv thaiv kab mob rau cov kab mob microbial thiab kev poob ntawm cov txiaj ntsig taxa [140]. Piv txwv li, kev sib xyaw ua ke ntawm meropenem, gentamicin, thiab vancomycin tau nce ntau ntawm pathobionts, xws li Enterobacteriaceae, thiab txo qis butyrate-producing commensals, xws li Bifidobacterium [141]. Cov kev soj ntsuam zoo sib xws tau pom thaum cov tshuaj tua kab mob hauv qhov ncauj txo qis cov kab mob probiotic hauv microbiota [142]. Nws kuj tau tshaj tawm tias ciprofloxacin txo qis qhov nplua nuj thiab ntau haiv neeg ntawm plab hnyuv microbiota nrog kev hloov hauv Bacteroidetes, Lachnospiraceae, thiab Ruminococcaceae [143]. Kev raug tshuaj tua kab mob cuam tshuam rau lub cev tiv thaiv kab mob, thiab qhov no txuas nrog kev hloov pauv microbiota. Piv txwv li, kev tshawb fawb hauv nas tau pom tias kev hloov pauv ntawm cov tshuaj tua kab mob hauv microbiota hloov Th1/Th2 tshuav nyiaj li cas rau Th2-kev tiv thaiv tseem ceeb, uas txo cov lymphocytes [144]. Cov kev tshawb pom zoo sib xws tau pom nyob rau hauv cov me nyuam mos macaques tom qab kev siv tshuaj tua kab mob hauv lub neej thaum ntxov uas ua rau cov tsiaj muaj kev phom sij rau cov kab mob ntsws, nrog rau neutrophil senescence, hyperinflammation, thiab macrophage dysfunction [145]. Thaum cov kev hloov pauv ntawm cov kab mob microbial tom qab kev kho tshuaj tua kab mob sib txawv [141,146], lub ntsiab lus tsis tu ncua zoo li lub sijhawm luv (thiab qee zaum, mus sij hawm ntev) poob ntawm qee yam keystone taxa thiab SCFA-ua cov kab mob [141,147]. Raws li tau hais tseg hauv Tshooj 5.1, SCFAs txhawb CD4+ T hlwb thiab ILCs los tsim cov tshuaj tiv thaiv IL-22 los ntawm ntau lub tshuab [80], suav nrog inhibition ntawm HDAC thiab stimulation ntawm GPR41/43 [106]. SCFAs kuj tseem tswj cov kab mob epithelial barrier muaj nuj nqi [148]. Cov ntawv ceeb toom tsis tu ncua qhia tau hais tias cov tshuaj tua kab mob txo qis SCFA qib [149–151]. Zuag qhia tag nrho, kev siv tshuaj tua kab mob ntau ntxiv hauv cov menyuam mos thiab cov neeg laus qhia tias cov teeb meem no yuav tshwm sim ntau dua los yog ntau dua yav tom ntej. Ceev faj siv cov tshuaj tua kab mob thiab kev tshawb fawb txuas ntxiv mus rau cov qauv thiab kev ua haujlwm ntawm lub plab microbiota yog qhov yuav tsum tau ua ua ntej los daws cov teeb meem no.
6.2. Fecal Microbiota Transplantation
Fecal microbiota transplantation (FMT) yog ib txoj hauv kev uas cov quav tau hloov ntawm ib tus neeg mus rau lwm tus. Lub hom phiaj yog los kho eubiosis los ntawm kev qhia cov txiaj ntsig zoo rau kev thim rov qab plab microbiota dysbiosis thiab rov ua kom lub cev tsis muaj zog. FMT tau tsim nws tus kheej raws li kev kho mob dav dav rau kev rov kis mob C. difficile [152]. Cov ntaub ntawv tsis ntev los no qhia tias FMT kuj tseem tuaj yeem ua tau zoo hauv kev kho mob hom I ntshav qab zib mellitus thiab IBD [153–156]. Kev tshawb fawb tsis tu ncua yog tshawb xyuas lub peev xwm ntawm FMT nyob rau hauv ntau yam ntawm lwm yam kab mob nrog tsim kev sib txuas rau plab microbiota dysbiosis, nrog rau cov kab mob cardiometabolic, kab mob autoimmune, pw tsaug zog apnea, kev nyuaj siab, thiab schizophrenia [157-161]. Ob peb lub tswv yim tau hais txog cov txiaj ntsig ntawm FMT. Ib qho piv txwv suav nrog Gram-negative anaerobic kab mob Bacteroides fragilis (B. fragilis). B. fragilis muaj ib qho txawv txav ntawm cov genomic DNA uas tau siv los tsim cov capsular polysaccharides, uas paub tias yog qhov tseem ceeb ntawm kev ua phem. Ntawm yim capsular polysaccharides loci ntawm B. fragilis, muaj ob lub capsular polysaccharides uas muaj zwitterionic nqi motif [162]. Ib txoj kev tshawb fawb tsis ntev los no tau pom tias B. fragilis thiab nws cov metabolite polysaccharide A (ib qho ntawm cov zwitterionic polymers) muaj peev xwm rov qab ua haujlwm tsis zoo Th1/Th2 tshuav nyiaj li cas hauv cov nas tsis muaj kab mob los ntawm TLR2-kev ua haujlwm nruab nrab ntawm NF-κB [163 ]. Nws yog polysaccharide lub dual-charge structural motif uas confers lub peev xwm no [164,165]. Lwm qhov piv txwv ntawm FMT suav nrog kev sib npaug ntawm Th17 thiab Treg cov pej xeem raws li pom hauv cov neeg mob colitis [166]. Tsis tas li ntawd, kev kho dua tshiab ntawm SCFA qib yog ib qho ntawm lwm cov txheej txheem ntawm cov txiaj ntsig ntawm FMT, raws li qhia nrog kev mob stroke rov qab [167]. Raws li tuaj yeem xav tau, cov tshuaj tua kab mob hauv cov kab mob dav dav tuaj yeem cuam tshuam qhov txiaj ntsig zoo ntawm FMT, raws li pom hauv cov piglets ua ntej nrog NEC [168]. Txawm hais tias muaj ntau qhov txiaj ntsig zoo ntawm FMT tau hais, nws yog ib qho tseem ceeb kom lees paub tias FMT tuaj yeem ua rau muaj kev hloov pauv ntawm cov kab mob pathogenic microbes tam sim no hauv cov quav pub rau tus neeg mob hloov, uas tuaj yeem ua rau mob sepsis thiab lwm yam kab mob [8,169].
6.3. Khoom noj khoom haus-, Probiotic-, thiab Prebiotic-Induced Microbiome Alterations
Lub plab microbiome muaj ntau yam kev ua haujlwm hauv metabolic, suav nrog metabolizing lipids, carbohydrates, thiab proteins. Ntau qhov kev tshawb fawb tsis ntev los no tau tsom tshwj xeeb rau kev sib txuas ntawm microbiome thiab kev noj haus. Khoom noj khoom haus additives, xws li emulsifying tus neeg sawv cev, ubiquitous nyob rau hauv cov zaub mov ua tiav heev, ua kom tus tswv mob o los ntawm kev hloov lub plab microbiome [170]. Ntawm qhov tod tes, Mediterranean-style noj zaub mov nce qib ntawm SCFA-ua cov kab mob thiab txo qis qhov mob [171]. Tsis tas li ntawd, cov zaub mov tsis muaj rog vegan txhim kho insulin rhiab heev thiab lub cev muaj pes tsawg leeg hauv cov neeg laus rog los ntawm kev hloov pauv ntawm Bacteroides thiab lwm yam kab mob hauv plab [172]. Lwm yam kev noj haus, xws li kev noj zaub mov muaj protein ntau, muaj kev txwv tsis pub muaj cov kab mob microbiota [173]. Hauv qab no, peb qhia meej meej txog lwm qhov kev noj haus uas tuaj yeem muaj qhov tsis zoo lossis muaj txiaj ntsig zoo rau lub plab microbiota-immune axis.
cistanche tubulosa- txhim kho lub cev tiv thaiv kab mob
6.3.1. Kev Noj Qab Haus Huv Siab
Kev noj zaub mov muaj ntsev ntau (HSD) cuam tshuam nrog cov kab mob metabolic, xws li kub siab thiab rog. Kev noj ntsev ntau dua 20% ntawm cov nyiaj pub dawb txhua hnub yog suav tias yog kev noj ntsev ntau. Ntsev, tshwj xeeb tshaj yog sodium, ua lub luag haujlwm tseem ceeb hauv kev tswj hwm homeostasis. Sodium cov ntsiab lus hauv cov ntshav tswj cov ntshav ntim; ntsev ntau dua nce ntshav ntim, thiab, yog li ntawd, nce ntshav siab [174]. Sib nrug los ntawm nws cov kev cuam tshuam ncaj qha rau hemodynamics, kev noj ntsev ntau tuaj yeem hloov kho lub plab microbiota, uas, dhau los, ua rau muaj kev cuam tshuam metabolic. Cov nyhuv ntawm HSD ntawm lub plab microbial muaj pes tsawg leeg tau tshaj tawm nyob rau hauv ntau tus qauv nas ntawm ntau yam kab mob [175–178]. Kev tshawb fawb los ntawm Hu et al. qhia tau tias kev noj ntsev ntau ntev ua rau enteric dysbiosis; Tshwj xeeb, feem pua ntawm Actinobacteria, Firmicutes, thiab Bacteroidetes tau hloov pauv ntau, thiab HSD ua rau lub plab xau, raum raug mob, thiab systolic ntshav siab [178]. Lwm txoj kev tshawb fawb tsis ntev los no tau qhia tias kev tswj hwm HSD rau cov nas rau 3 lub lis piam ua rau muaj kev nce ntxiv hauv Firmicutes / Bacteroidetes (F / B) piv thiab Proteobacteria [179], ob qho tib si yog cov cim classic ntawm plab microbiota dysbiosis thiab cuam tshuam nrog cov kab mob metabolic. Ib yam li ntawd, lwm txoj kev tshawb fawb pom tias HSD nce qhov F / B piv thiab kev nplua nuj ntawm Lachnospiraceae thiab Ruminococcus tab sis txo qis ntawm Lactobacillus [177]. Daim ntawv qhia los ntawm Miranda et al. qhia ntxiv tias HSD txo Lactobacillus spp. thiab butyrate ntau lawm hauv tus qauv colitis nas [175]. Ntxiv nrog rau kev hloov pauv microbiota, ntsev tuaj yeem cuam tshuam rau lub cev tiv thaiv kab mob. Cov ntsiab lus tseem ceeb ntawm ntsev, piv txwv li, sodium chloride (NaCl), induces pathogenic Th17 hlwb (IL-17- tsim T pab hlwb) hauv tib neeg thiab nas naïve CD4+ T cell kab lis kev cai hauv vitro [180] . Ib yam li ntawd, HSD txhim kho TNF- thiab IL-17A hauv ap38- nyob ntawm tib neeg lamina propria mononuclear hlwb [181] thiab txhawb txoj hnyuv Th17 cov lus teb tab sis inhibited txoj haujlwm ntawm Treg hlwb [182], tag nrho cov uas exacerbated qhov hnyav ntawm colitis nyob rau hauv nas. Tsis tas li ntawd, kev noj zaub mov ntxiv ntsev ntxiv txhawb nqa Th17 hlwb thiab pro-inflammatory cytokines GM-CSF, TNF- , thiab IL-2, uas tau ua HSD ib puag ncig kev pheej hmoo rau kev loj hlob ntawm cov kab mob autoimmune [183]. Ua ke, kev noj ntsev ntau yog suav tias yog kev puas tsuaj vim tias nws ua rau muaj kev cuam tshuam tsis zoo rau lub plab microbiota thiab txhawb nqa cov neeg kho kom zoo.
6.3.2. Khoom noj khoom haus Polyphenols
Kev noj zaub mov polyphenols kuj tau paub ntau ntxiv rau lawv cov teebmeem ntawm plab microbiota. Cov micronutrients no, suav nrog, tab sis tsis txwv rau, flavonoids, anthocyanins, catechins, thiab tannins, tuaj yeem pom hauv ntau yam khoom noj thiab dej haus, xws li zaub, txiv hmab txiv ntoo, kas fes, thiab tshuaj yej. Txawm hais tias tsuas yog ib feem ntawm polyphenols tau nqus hauv cov hnyuv [184], ib qho loj dua uas tsis tau nqus tau nyob hauv plab thiab txhawb kev loj hlob ntawm cov kab mob uas tau xaiv [185]. Piv txwv li, epigallocatechin-3-gallate (EGCG; ib tug loj catechin nyob rau hauv ntsuab tshuaj yej) txhawb txoj kev loj hlob ntawm cov Bacteroides thiab Bifidobacterium thiab suppresses lub paj ntawm pathogenic Fusobacterium, Bilophila, thiab Enterobacteriaceae [186]. Xws li cov teebmeem microbiota-modulating ntawm EGCG tau sau tseg los tiv thaiv colitis [187], kev noj zaub mov muaj roj ntau vim rog rog [188–190], hluav taws xob-induced mucositis [191], thiab Clostridium difficile infection (CDI) [192] hauv cov nas. . Txawm hais tias EGCG cuam tshuam li cas microbiota tsis to taub zoo, ntau qhov kev tshawb fawb qhia tias nws tuaj yeem yog vim muaj cov kab mob bactericidal ntawm EGCG, piv txwv li, (i) tsim H2O2 uas ua rau cov kab mob ntawm phab ntsa puas lawm [193,194], (ii) inhibiting kab mob fatty acid. thiab folate biosynthesis [195,196], thiab (iii) inducing oxidative kev nyuaj siab thiab reactive oxidative hom (ROS) tsim nyob rau hauv cov kab mob susceptible [197]. Cov txiaj ntsig zoo ntawm polyphenols, ib sab ntawm EGCG, ntawm plab microbiota kuj tau sau tseg thiab tuaj yeem raug xa mus rau hauv kev tshuaj xyuas los ntawm Plamada thiab Vodnar [198]. Ua ke, kev nce qib hauv cheeb tsam kev tshawb fawb no pab qhia txog tshuaj yej thiab lwm yam khoom noj uas muaj polyphenol-nplua nuj raws li cov txheej txheem tshiab ntawm prebiotics.
6.3.3. Probiotics, Prebiotics, thiab Dietary Fiber
Muaj ntau txoj kev tshawb fawb txog kev siv probiotics thiab prebiotics thiab kawm txog lawv cov teebmeem ntawm microbiome muaj pes tsawg leeg. Probiotics, uas feem ntau suav nrog cov kab mob xws li Lactobacillus, Bifidobacteria, thiab cov poov xab, tswj kev ncaj ncees ntawm txoj hnyuv epithelial barrier los ntawm kev txo qis ntawm LPS, tiv thaiv nruj junctions, thiab txo qis ntawm pro-inflammatory cytokines [199,200]. Rau ib qho piv txwv tshwj xeeb, Lactobacillus johnsonii probiotic supplementation rau dams stabilized ob niam txiv thiab cov xeeb ntxwv plab microbiota thiab tiv thaiv cov menyuam mos los ntawm tus kab mob retroviral vim muaj tsawg dua Th2 lub cev tiv thaiv kab mob [201]. Tsis ntev los no, nws tau pom tias Peyer's thaj ua rau thaj txhim kho thiab xa cov probiotic (xws li, L. reuteri) cov cim rau CCR6- nthuav tawm cov kab mob ua ntej-zoo li B hlwb, txhawb lawv qhov sib txawv thiab autocrine TGF -1 ua kom muaj zog; qhov no ua rau induction ntawm PD-1-qhia Th1-dependent IgA, txo cov plab hnyuv microbiota dysbiosis, thiab tiv thaiv kab mob hauv plab [202]. Prebiotics, suav nrog cov khoom noj khoom haus xws li inulin, fructooligosaccharides, thiab galactooligosaccharides, xaiv ntau tus neeg probiotics, feem ntau Lactobacillus thiab Bifidobacteria. Kev noj cov fiber ntau ntxiv, tshwj xeeb tshaj yog fructans thiab galactooligosaccharides, nce qhov kev nplua nuj ntawm Bifidobacterium thiab Lactobacillus spp. tsis hloov pauv -diversity [203]. Ib txoj kev tshawb fawb tau pom tias thaum nas noj cov zaub mov noj tau hloov mus rau cov khoom noj uas muaj cov nroj tsuag, muaj qhov nce ntxiv hauv Bacteroides thiab Alloprevotella thiab txo qis hauv Porphyromonadaceae thiab Erysipelotrichaceae [204]. Ib yam li ntawd, tib neeg ntawm kev noj zaub mov zoo li yuav muaj cov pej xeem ntau dua ntawm Prevotella thiab muaj feem cuam tshuam nrog kev cuam tshuam rau lub plab tsis zoo, xws li IBD [2,205,206]. Ob leeg pro- thiab prebiotics nce SCFA qib, muaj txiaj ntsig zoo rau kev tiv thaiv kab mob hauv ntau txoj hauv kev, suav nrog kev cuam tshuam ntawm cov kab mob pro-inflammatory NF-κB thiab induction ntawm Treg hlwb [107,207]. Cov txiaj ntsig sib koom ua ke ntawm pro- thiab prebiotics piav qhia lawv txoj kev vam meej hauv kev txo qis qee yam metabolic, tsis haum, thiab kab mob autoimmune txuas rau plab microbiota dysbiosis [200,208-211]. Txawm li cas los xij, nws yog ib qho tseem ceeb uas yuav tsum lees paub tias cov tshuaj probiotics tsuas yog ua haujlwm thaum ua haujlwm nquag thiab tsis muaj pov thawj cov txiaj ntsig ntev. Qhov no muaj feem xyuam rau cov kev paub tsawg txog ntev npaum li cas probiotic prophylaxis tuaj yeem txhim kho lub plab microbiota hauv cov menyuam mos yug ntxov uas muaj kev pheej hmoo ntau dua rau cov kab mob inflammatory [212]. Txawm hais tias tsis tshua muaj, probiotic microbes lawv tus kheej tuaj yeem ua rau muaj kab mob thiab endotoxemia (Lactobacillus spp.), lossis cov kev mob tshwm sim tsis zoo tuaj yeem tshwm sim los ntawm kev kis kab mob (Mucormycetes) [8]. Cov kev xav zoo sib xws thiab kev txhawj xeeb yuav tsum tau siv rau prebiotics thiab.
7. Kev ua txhaum ntawm Microbiome–Immunity Interaction nyob rau hauv ntau yam kab mob
7.1. Gut Microbiota Dysbiosis thiab Immune Dysregulation
Lub plab epithelial hlwb thiab mucosa ua haujlwm tiv thaiv lub cev tiv thaiv kab mob thiab endotoxemia. Lub plab microbiota metabolites, xws li SCFA thiab lwm cov kua tsib acids, kuj tswj lub plab permeability ntawm immunomodulation. Ntawm qhov kev ceeb toom, lwm lub plab-microbiota-derived metabolite inosine, tsim los ntawm Bifidobacterium thiab A. muciniphila, ua kom Th1 sib txawv thiab cov txiaj ntsig ua haujlwm ntawm naïve T hlwb [213]. Gut-microbiota-mediated immune teb yog qhov tseem ceeb rau kev tiv thaiv txoj hnyuv permeability. Nws yog hypothesized tias plab microbiota dysbiosis nce plab hnyuv permeability los ntawm ib tug 'leaky plab,' uas tso cai rau opportunistic kab mob thiab lawv cov microbial cov khoom / coxins mus txeeb cov hlab ntsha thiab thaum kawg mount ib inflammatory teb [214–216]. Kev txhawb nqa rau lub tswv yim no los ntawm ntau cov metabolites paub, xws li phenolic thiab sulfur-muaj cov khoom sib txuas, uas tuaj yeem ua mob rau lub plab hnyuv epithelia [217], cuam tshuam kev sib tshuam ntawm cov cellular kaw [218], thiab txhawb cov kab mob translocation [219]. Cov txiaj ntsig no, uas tseem suav nrog kev tiv thaiv kab mob hauv lub cev tsis ua haujlwm thiab tsis muaj peev xwm tshem tawm cov kab mob nkag mus, ua rau cov kab mob inflammatory [220,221]. Tshooj lus ntawm qhov kev tshuaj xyuas no yuav tham txog cov kab mob microbiota-immune axis nyob rau hauv cov kab mob hauv plab thiab cov kab mob hauv plab (Daim duab 2 thiab Table 1).
Daim duab 2. Gut microbiota dysbiosis ua rau muaj ntau yam pathophysiological. Lub plab microbiota dysbiosis tuaj yeem tshwm sim los ntawm kev noj zaub mov, tshuaj tua kab mob, thiab caj ces. Lub plab microbiota dysbiosis tuaj yeem ua rau thiab txhawb nqa cov qog nqaij hlav, xws li mob qog nqaij hlav hauv plab thiab cov kab mob siab hepatocellular, nrog rau cov kab mob inflammatory, mob autoimmune, thiab cardiometabolic. Gut microbiota dysbiosis-induced immune dysregulation yog lwm yam etiological rau cov kab mob ntawm ntau lwm cov npe, suav nrog hnub nyoog, poj niam txiv neej, thiab tshuaj.
Table 1. Cov ntsiab lus ntawm lub plab microbiota–Immune axis nyob rau hauv ntau yam kab mob.
