Lub luag haujlwm ntawm Gut Microbiota hauv cov menyuam yaus uas muaj mob raum

Abstract:Kev cuam tshuam ntawm cov muaj pes tsawg leeg thiab cov qauv ntawm lub plab microbiota, uas yog dysbiosis, dictates lub pathophysiology ntawmkab mob raum. Lub bidirectionallub raum - lub plab axisyog txaus siab raumob raum mob(CKD); tusuremic uacoj mus rauplab hnyuv dysbiosisthiab plab hnyuv microbial metabolites thiab co toxins cuam tshuam rau hauvpoob ntawm lub raum ua haujlwmthiabnce comorbidity nra. Xav txog qhov ntawdkab mob raumtuaj yeem tshwm sim hauv menyuam yaus lossis txawm tias ntxov hauv lub neej hauv plab, kev txheeb xyuas ntawm cov kab mob sib txuas ntawmplab hnyuv microbiota dysbiosisthiab kev loj hlob ntawm cov kab mob raum rau menyuam yaus tsim nyog tau txais kev saib xyuas ntau dua. Qhov kev tshuaj xyuas no tsom rau cov kab mob sib txuas ntawm dysbiotic plab microbiota thiab cov kab mob raum rau menyuam yaus, suav nrogCKD, hloov raum, hemodialysisthiabperitoneal lim ntshav, thiab idiopathic nephrotic syndrome. Cov kev kho mob plab microbiota-targeted nrog rau kev noj zaub mov, probiotics, prebiotics, postbiotics, thiab fecal microbial transplantation yog tham txog lawv lub peev xwm rau kev kho mob.pediatric mob raum. Kev nkag siab tob dua ntawm plab microbiota hauv cov kab mob hauv lub raum rau menyuam yaus yuav pab tsim kho lub plab microbiota-targeted kev cuam tshuam rau kev tiv thaiv lossis txo qis lub nra thoob ntiaj teb.kab mob raum. 

Nyem qhov no kom tau txais TOP-QUALITY CISTANCHE RAU ​​RENAL DISEASES

1. Taw qhia

Peb lub plab hnyuv muaj trillions ntawm microbes hu ua plab microbiota. Cov plab hnyuv microbes tau koom tes nrog tib neeg rau kev sib koom ua ke muaj txiaj ntsig zoo thiab koom nrog kev noj qab haus huv thiab kab mob [1]. Lub shaping ntawm lub plab microbiome pib thaum yug los, thaum kev hloov kho ntawm nws cov muaj pes tsawg leeg feem ntau yog nyob ntawm ntau yam nyob rau hauv lub neej thaum ntxov [2]. Kev cuam tshuam hauv kev muaj pes tsawg leeg thiab kev ua haujlwm ntawm lub plab microbiota tuaj yeem cuam tshuam txoj hnyuv permeability, microbial-derived metabolites, thiab tiv thaiv kab mob, yog li ua rau lub plab dysbiosis [3].

Cov kab mob raum rau menyuam yaus muaj xws li cov kab mob dav dav uas cuam tshuam rau kev txav mus los thiab kev tuag tom qab lub neej. Txij li thaum cov neeg laus cov kab mob hauv lub raum tuaj yeem tshwm sim hauv fetal lub neej thiab menyuam yaus [4,5], Ntiaj Teb Lub Raum Hnub 2016 tau ceeb toom rau pej xeem rau kev saib xyuas tshwj xeeb tsim nyog rau cov kab mob raum menyuam [6]. Cov pov thawj tseeb thiab kev sim tshuaj ntsuam xyuas tau ntxiv dag zog rau kev koom tes ntawm ntau yam ntawm lub neej thaum ntxov thiab kev loj hlob ntawm cov kab mob raum tom qab hauv lub neej [4,5]. Txawm hais tias tag nrho cov txheej txheem tseem tsis tau lees paub, cov pov thawj tam sim no qhia tias lub plab microbiota dysbiosis tau tshwm sim los ua ib qho kev sib txuas ntawm cov kab mob hauv lub raum thiab cov xwm txheej cuam tshuam [7-10].

Qhov kev sib txuas ntawm ob sab ntawm lub raum kab mob thiab plab microbiota yog hu ua lub raum- plab axis [11]. Hauv cov neeg laus, kev tshawb fawb ua ntej tau npaj qee cov txheej txheem txuas cov plab hnyuv microbiota dysbiosis rau cov kab mob hauv lub raum, suav nrog o, plab barrier tsis ua haujlwm, hloov pauv ntawm microbiota muaj pes tsawg leeg, tiv thaiv kab mob, sib sau ntawm trimethylamine N-oxide (TAMO), dysregulated luv-chain fatty acids (SCFAs) thiab lawv cov receptors, thiab uremic toxins [7–10]. Txawm li cas los xij, muaj cov ntaub ntawv tsis txaus ntseeg txog yuav ua li cas lub raum-lub plab axis cuam tshuam rau cov kab mob hauv lub raum thiab qhov cuam tshuam ntawm plab dysbiosis yog li cas hauv kev hloov pauv cov txheej txheem pathological [8].

Tau ntau xyoo, kev kho mob plab hnyuv microbiota suav nrog prebiotics, probiotics, thiab postbiotics tau txais kev saib xyuas vim lawv cov txiaj ntsig kev noj qab haus huv [12,13]. Xav tias plab microbiota dysbiosis yog koom nrog hauv cov kab mob ntawm ntau lub raum kab mob, nws zoo nkaus li tsim nyog rau lub plab microbiota rau kev tiv thaiv thiab kho cov kab mob hauv lub raum. Lub hom phiaj ntawm peb qhov kev tshuaj xyuas yog los muab kev pom rau kev sib raug zoo ntawm plab microbiota thiab microbial metabolites nyob rau hauv pathophysiology ntawm cov menyuam yaus lub raum kab mob thiab hloov kho lub plab microbiota raws li txoj hauv kev kho mob.

2. Lub raum-Gut Axis

2.1. Gut Microbiota yog dab tsi?

Lub plab microbiota muaj ntau txhiab tus kab mob microbial, thiab trillions ntawm cov kab mob hauv nruab nrab tib neeg lub plab hnyav txog 1 kg. Lub plab microbes cuam tshuam rau kev nqus, metabolism, thiab khaws cia cov khoom noj khoom haus, nrog rau kev cuam tshuam loj hauv kev txiav txim siab tus tswv lub cev [1]. Tsis tas li ntawd, cov plab hnyuv microbiota thiab nws cov metabolites ua haujlwm tshwj xeeb hauv tus tswv, suav nrog kev saib xyuas lub plab mucosal barrier, immunomodulation, tshuaj metabolism, kev tswj ntshav siab (BP), thiab tiv thaiv kab mob.

Microbial diversity raug soj ntsuam raws li ob qhov tsis muaj: - thiab -diversity. Qhov -diversity yog variation nyob rau hauv ib tug qauv thiab yog siv los piav txog cov compositional complexity, whereas -diversity txhais tau hais tias cov taxonomical sib txawv ntawm cov qauv. Lub plab microbiota yog tsim los ntawm cov kab mob sib txawv ntawm cov kab mob taxonomically cais los ntawm genus, tsev neeg, kev txiav txim, thiab phyla [14]. Feem ntau, lub plab microbiota noj qab nyob zoo yog feem ntau tsim los ntawm phyla Firmicutes thiab Bacteroidetes, ua raws li Actinobacteria thiab Verrucomicrobia. Cov yam ntxwv ntawm lub plab microbiota yog qhov sib txawv thiab sib txawv ntawm cov tib neeg, thiab txawm hais tias cov microbiota paub tab yog qhov zoo, nws tuaj yeem hloov pauv los ntawm ob qho tib si sab hauv thiab sab nraud stimuli. Cov cim ntawm microbial stability, xws li ntau haiv neeg thiab kev nplua nuj, feem ntau yog siv los ua cov cim qhia ntawm plab noj qab haus huv vim lawv cov koom haum nrog ntau cov kab mob ntev [1].

Lub plab microbiota txawv ntawm tib neeg thiab hloov pauv thaum lub sijhawm tib neeg lub neej, nyob rau hauv kev cuam tshuam ntawm yam xws li kev noj haus, ib puag ncig, tshuaj, thiab kab mob [15]. Kev noj haus yog qhov tseem ceeb cuam tshuam rau lub plab microbiota [15]. Cov khoom noj khoom haus-derived microbial metabolites, tshwj xeeb tshaj yog SCFAs, TMAO, tryptophan derivatives, branched-chain amino acids, thiab bile acids, tau muaj kev cuam tshuam rau cov kab mob ntawm cov kab mob metabolic. Dietary fiber yog fermented los ntawm plab microbes, ua SCFAs [16]. SCFAs, thiab tshwj xeeb tshaj yog butyrate, koom nrog hauv kev khaws cov kab mob hauv plab hnyuv homeostasis thiab tiv thaiv cov lus teb tiv thaiv oxidation thiab o [16]. SCFAs tuaj yeem ncaj qha qhib G-coupled receptors los tswj ntau yam txheej txheem physiological. Cov SCFA receptors no tau qhia nyob rau hauv lub raum thiab tau tshaj tawm tias ua haujlwm raws li kev tswj hwm ntshav siab (BP). Kev noj zaub mov L-carnitine thiab choline, uas pom muaj feem ntau hauv cov khoom noj tsiaj, tuaj yeem metabolized rau trimethylamine (TMA). TMA yog metabolized rau TMAO, uas yog tom qab hloov mus rau dimethylamine (DMA) [17]. High TMAO tau txuas rau kev pheej hmoo ntawm cov hlab plawv thiab txhua qhov ua rau tuag [17].

Qee qhov microbiota-derived tryptophan metabolites yog uremic toxins, feem ntau yog los ntawm txoj hauv kev indole thiab kynurenine [18]. Ntau indole derivatives xws li Indoxyl sulfate (IS) thiab indoleacetic acid (IAA) yog acyl hydrocarbon receptor (AHR) ligands, muaj pro-inflammatory, prooxidant, procoagulant, thiab pro-apoptotic teebmeem [19]. Nws paub tias AHR tuaj yeem hloov kho T tus pab 17 cell (TH17) thiab T regulatory cell axis, uas koom nrog hauv plab homeostasis thiab lub cev tiv thaiv kab mob [20]. Ua ke, cov kev tshawb pom no ua rau lub plab microbiota muaj kev cuam tshuam thoob ntiaj teb rau kev ua haujlwm ntawm lub cev.

2.2. Lub raum-Gut Axis hauv CKD

Cov kev tshawb fawb ntawm tib neeg thiab kev sim txhawb nqa tias lub raum-lub plab axis koom nrog cov kab mob ntawm ntau yam kab mob raum. Ib qho piv txwv yog kev tshawb fawb paub zoo hauv kab mob raum (CKD). Muaj kev sib raug zoo ntawm lub plab microbiota thiab CKD [11]. CKD tuaj yeem cuam tshuam rau lub plab microbiota hauv ntau txoj hauv kev. Ua ntej, CKD yog nrog los ntawm kev nce plab hnyuv permeability, uas yog lub plab hnyuv [21]. Cov kab mob thiab lawv cov khoom siv phab ntsa ntawm tes xws li lipopolysaccharide (LPS) tuaj yeem hloov pauv ntawm lub plab lumen mus rau hauv cov hlab ntsha. Kev nkag mus ntawm cov kab mob thiab LPS rau hauv cov hlab ntsha tuaj yeem ua rau lub cev tiv thaiv kab mob hauv lub cev los ntawm kev hu xov tooj zoo li tus neeg txais xov tooj 4 (TLR4)-raws li kev ua haujlwm, ua rau lub raum mob. Raws li txoj cai, lub plab khoob ua rau mob, tsis muaj zaub mov noj thiab ua kom CKD nce ntxiv [21,22]. Qhov thib ob, uremic toxins yog tsim nyob rau hauv cov neeg mob CKD thiab cuam tshuam rau kev loj hlob ntawm plab hnyuv microbes. Tsawg kev nplua nuj (sawv cev los ntawm -diversity) ntawm plab microbiota tau tshaj tawm hauv cov neeg mob raum kawg (ESKD) ntau dua li hauv cov kev tswj hwm [23]. Kev ua haujlwm ua ntej tau qhia tias cov neeg mob CKD tau nthuav tawm qis dua ntawm cov kab mob muaj txiaj ntsig zoo xws li Bifidobacterium thiab Lactobacillus hom [24]. Tsis tas li ntawd, kev hloov pauv ntawm cov plab hnyuv microbial taxa hauv cov neeg mob nrog CKD tau txheeb pom [23]. Tsis tas li ntawd, ntau yam CKD muaj feem cuam tshuam nrog dysbiotic plab hnyuv microbiota, suav nrog kev noj fiber ntau tsawg, noj tsis txaus, metabolic acidosis, kev siv tshuaj tua kab mob / tshuaj, nce plab hnyuv tawm ntawm urea, tsub zuj zuj ntawm cov co toxins, thiab txo lub plab motility [7-11. ].

Ntawm qhov tod tes, plab hnyuv microbiota-derived metabolites koom nrog CKD kev loj hlob thiab comorbidity. Cov teebmeem microbial metabolite muaj xws li (1) microbial fermentation ntawm kev noj haus fibers los tsim SCFAs uas txhim kho SCFA receptors, nce zog siv nyiaj thiab inhibit histone deacetylase (HDAC) kev ua; (2) microbial hloov dua siab tshiab ntawm tryptophan-derived uremic toxins nrog rau IS thiab p-cresyl sulfate (PCS), uas dysregulate Treg / TH17 tshuav nyiaj li cas los ntawm AHR activation thiab tom qab ntawd accelerate CKD kev loj hlob; thiab (3) microbial hloov dua siab tshiab ntawm choline rau TMA, uas yog tom qab hloov mus rau TMAO, paub zoo txog CVD kev pheej hmoo. Peb tau piav qhia txog cov kev sib raug zoo no hauv daim duab 1.

2.3. Lub raum-Gut Axis hauv Lwm Cov Kab Mob Raum

Cov kab mob hauv lub raum tsis zoo nrog cov kab mob dysbiotic gut microbiota kuj cuam tshuam rau lwm cov kab mob raum, suav nrog mob raum raug mob (AKI) [25], hloov raum (KT) [26], kab mob urinary pob zeb [27], kab mob urinary tract ( UTI) [28], thiab mob qog noj ntshav genitourinary [29].

2.3.1. Mob raum mob

Piv rau CKD, qee qhov kev tshawb fawb tau tshawb xyuas qhov sib txawv ntawm lub raum thiab lub plab hauv AKI. Hauv kev raug mob ischemia / reperfusion (IRI) nas qauv, lub plab microbiota dysbiosis, tus cwj pwm los ntawm kev txo qis hauv Ruminococcaceae thiab Lactobacilli thiab nce hauv Enterobacteriaceae, muaj nyob rau hnub 1 [30]. Lwm txoj kev tshawb fawb tau pom tias cov nas tsis muaj kab mob tau txais cov quav los ntawm IRI nas muaj mob raum mob hnyav dua piv rau kev tswj hwm. Yog li, AKI tuaj yeem ua rau lub plab dysbiosis nyob rau lub sijhawm luv luv, thiab kev hloov pauv ntawm cov kab mob microbial tuaj yeem txiav txim siab tom qab AKI qhov hnyav [30].

2.3.2. Lub raum Transplantation

Tsis zoo li CKD, cov neeg mob KT muaj kev txhim kho hauv lub raum ua haujlwm, muab tso rau hauv cov theem ua ntej ntawm CKD. Txawm li cas los xij, kev ua haujlwm yav dhau los tau tshaj tawm tias KT tseem tuaj yeem ua rau muaj kev hloov pauv loj hauv cov kab mob microbial [31]. Nyob rau hauv kev pom ntawm cov kev kho mob nyuaj dua ntawm KT cov neeg tau txais kev pab, xws li kev tswj hwm cov tshuaj tiv thaiv kab mob, cov teeb meem tom qab hloov pauv thiab siv cov tshuaj tua kab mob ntau zaus, lub raum tsis zoo ntawm lub raum - lub plab axis tseem nyob thiab tsim nyog tau txais kev soj ntsuam ntxiv.

Daim duab 1. Daim duab qhia txog cov txheej txheem tom qab lub raum-lub plab axis txuas plab microbiota dysbiosis mus rau mob raum kab mob (CKD). LPS=lipopolysaccharide; TLR4=tus xov tooj zoo li tus neeg txais xov tooj 4; SCFA=luv-chain fatty acid; YOG=indoxyl sulfate; PCS=p-cresyl sulfate; Th17=T-helper 17 cell; Treg=tswj T cell; AHR=aryl hydrocarbon receptor; TMAO=trimethylamine-N-oxide; TMA=trimethylamine

2.3.3. Urinary Stone Disease

Txawm hais tias tus kab mob urinary pob zeb tsis tshua muaj nyob rau hauv cov menyuam yaus, kev sib raug zoo ntawm plab microbiota thiab nephrolithiasis tau pom nyob rau hauv cov neeg laus (27]. Kev tshawb fawb meta. Prevotellacene, thiab Roseburia thiab nce hauv Enterobac-feriacene thiab Strepfococcacene (27. Muab hais tias tso zis ntau ntawm oxalate, calcium, thiab uric acid muaj lub luag haujlwm tseem ceeb hauv kev tsim pob zeb, nce net gastrointestinal absorption vim tsis muaj microbial degradation ntawm cov pob zeb muaj pes tsawg leeg tuaj yeem cuam tshuam. Calcium oxalate pob zeb yog hom pob zeb ntau tshaj plaws ntawm lub raum Tsis muaj oxalate-degrading microbes xws li Omlobacter formigenes tau txuas nrog kev tsim pob zeb (32]. Nyob rau hauv cov xwm txheej ntawm lub cev, ib feem peb ntawm uric acid yog tawm los ntawm txoj hnyuv, kuj qhia txog qhov muaj feem cuam tshuam ntawm plab microbiota hauv pathogenesis ntawm uric acid pob zeb. Ntau qhov kev soj ntsuam tau pom tias lub plab microbiota profile hauv cov neeg mob lub raum pob zeb yog qhov txawv ntawm qhov kev tswj hwm, uas ntxiv qhia tias lub plab microbiota muaj qhov tseem ceeb hauv kev tsim pob zeb (33].

2.3.4. Urinary Tract Infections Cov kab mob uropathogenic

Escherichia coli (UPECs) yog tus neeg sawv cev tseem ceeb ntawm UTIs. Cov kab mob UPEC no muaj ntau nyob rau hauv lub plab ntawm cov neeg mob nrog UTIs thiab yog li suav tias yog los ntawm lub plab [34]. Qhov kev xav no tau txhawb nqa los ntawm kev tshawb fawb yav dhau los qhia tias kev nce ntxiv ntawm E. coli hauv lub plab yog cuam tshuam nrog kev txhim kho yav tom ntej ntawm E. coli-induced UTI, thiab E. coli hom kab mob hauv cov zis tau zoo ib yam li cov neeg nyob hauv lub cev. lub cev los ntawm tib lub ntsiab lus [35]

2.3.5. Cov kab mob genitourinary

Ntxiv mus, lub peev xwm cuam tshuam ntawm plab microbiome ntawm pathobiology ntawm cov qog nqaij hlav genitourinary tau kawm ntau hauv cov neeg laus [29], txawm hais tias cov kab mob no tsis tshua muaj tshwm sim. Raws li ntau cov carcinogens raug tsim nyob rau hauv lub plab thiab lim los ntawm cov zis ua ntej excretion, cov kab mob plab yuav tsis tau tsuas yog koom nyob rau hauv txoj kev loj hlob ntawm genitourinary qog nqaij hlav, tab sis kuj ua raws li kev kho lub hom phiaj rau kev tiv thaiv ntawm cov qog nqaij hlav.

Supportive Service Ntawm Wecistanche-Qhov loj tshaj plaws cistanche exporter nyob rau hauv Tuam Tshoj:

Email: wallence.suen@wecistanche.com

Whatsapp / Tel: +86 15292862950

Khw:

https://www.xjcistanche.com/cistanche-shop