Talk:Human microbiota

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Wow[edit]

This review's coverage of microbiota-derived metabolite biosynthesis/pharmacodynamics is pretty comprehensive.[1] PMID 26531326 seems to cover the same topic - need to get access to it. Seppi333 (Insert ) 08:59, 27 June 2016 (UTC)

here Barbara (WVS) (talk) 08:59, 28 June 2016 (UTC)
Ah, thanks. Seppi333 (Insert ) 10:38, 28 June 2016 (UTC)
Diagram+reflist
Tryptophan metabolism by human gastrointestinal microbiota
Tryptophan metabolism diagram
This diagram shows the biosynthesis of bioactive compounds (indole and certain derivatives) from tryptophan by bacteria in the gut.[1] Indole is produced from tryptophan by bacteria that express tryptophanase.[1] Clostridium sporogenes metabolizes indole into 3-indolepropionic acid (IPA),[2] a highly potent neuroprotective antioxidant that scavenges hydroxyl radicals.[1][3][4] In the intestine, IPA binds to pregnane X receptors (PXR) in intestinal cells, thereby facilitating mucosal homeostasis and barrier function.[1] Following absorption from the intestine and distribution to the brain, IPA confers a neuroprotective effect against cerebral ischemia and Alzheimer’s disease.[1] Lactobacillus species metabolize tryptophan into indole-3-aldehyde (I3A) which acts on the aryl hydrocarbon receptor (AhR) in intestinal immune cells, in turn increasing interleukin-22 (IL-22) production.[1] Indole itself acts as a glucagon-like peptide-1 (GLP-1) secretagogue in intestinal L cells and as a ligand for AhR.[1] Indole can also be metabolized by the liver into indoxyl sulfate, a compound that is toxic in high concentrations and associated with vascular disease and renal dysfunction.[1] AST-120 (activated charcoal), an intestinal sorbent that is taken by mouth, adsorbs indole, in turn decreasing the concentration of indoxyl sulfate in blood plasma.[1]

References

  1. ^ a b c d e f g h i j Zhang LS, Davies SS (April 2016). "Microbial metabolism of dietary components to bioactive metabolites: opportunities for new therapeutic interventions". Genome Med. 8 (1): 46. doi:10.1186/s13073-016-0296-x. PMC 4840492Freely accessible. PMID 27102537. Lactobacillus spp. convert tryptophan to indole-3-aldehyde (I3A) through unidentified enzymes [125]. Clostridium sporogenes convert tryptophan to IPA [6], likely via a tryptophan deaminase. ... IPA also potently scavenges hydroxyl radicals 
    Table 2: Microbial metabolites: their synthesis, mechanisms of action, and effects on health and disease
    Figure 1: Molecular mechanisms of action of indole and its metabolites on host physiology and disease
  2. ^ Wikoff WR, Anfora AT, Liu J, Schultz PG, Lesley SA, Peters EC, Siuzdak G (2009). "Metabolomics analysis reveals large effects of gut microflora on mammalian blood metabolites". Proc. Natl. Acad. Sci. U.S.A. 106 (10): 3698–703. doi:10.1073/pnas.0812874106. PMC 2656143Freely accessible. PMID 19234110. Production of IPA was shown to be completely dependent on the presence of gut microflora and could be established by colonization with the bacterium Clostridium sporogenes. 
    IPA metabolism diagram
  3. ^ "3-Indolepropionic acid". Human Metabolome Database. University of Alberta. Retrieved 12 October 2015. Indole-3-propionate (IPA), a deamination product of tryptophan formed by symbiotic bacteria in the gastrointestinal tract of mammals and birds. 3-Indolepropionic acid has been shown to prevent oxidative stress and death of primary neurons and neuroblastoma cells exposed to the amyloid beta-protein in the form of amyloid fibrils, one of the most prominent neuropathologic features of Alzheimer's disease. 3-Indolepropionic acid also shows a strong level of neuroprotection in two other paradigms of oxidative stress. (PMID 10419516 )
    Origin:  • Endogenous  • Microbial
     
  4. ^ Chyan YJ, Poeggeler B, Omar RA, Chain DG, Frangione B, Ghiso J, Pappolla MA (1999). "Potent neuroprotective properties against the Alzheimer beta-amyloid by an endogenous melatonin-related indole structure, indole-3-propionic acid". J. Biol. Chem. 274 (31): 21937–42. doi:10.1074/jbc.274.31.21937. PMID 10419516. [Indole-3-propionic acid (IPA)] has previously been identified in the plasma and cerebrospinal fluid of humans, but its functions are not known. ... In kinetic competition experiments using free radical-trapping agents, the capacity of IPA to scavenge hydroxyl radicals exceeded that of melatonin, an indoleamine considered to be the most potent naturally occurring scavenger of free radicals. In contrast with other antioxidants, IPA was not converted to reactive intermediates with pro-oxidant activity. 

Metabolite table[edit]

Human microbiota-derived bioactive compounds
Metabolite Dietary source Taxonomic group or species
that produce the metabolite
Biological targets and
mechanism of action
Effects on human health and disease Sources
Acetic acid Dietary fiber Most anaerobic gut bacteria [1]
Butyric acid Dietary fiber Ruminococcaceae spp.
Lachnospiraceae spp.
Bacteroides spp.
Clostridium butyricum
Faecalibacterium prausnitzii
Colonocyte mitochondria (energy source)
•Class I histone deacetylases (1, 2, 3, 8) (inhibitor)
Niacin receptor 1 (full agonist)
Free fatty acid receptor 2 (full agonist)
Free fatty acid receptor 3 (full agonist)
•Improves intestinal barrier function
•Improves insulin sensitivity
•Increases energy expenditure
•Reduces lipogenesis (fat storage)
Anti-cancer (colon cancer)
Anti-inflammatory
[1][2][3]
[4][5]
Propionic acid Dietary fiber [1]
Indole Tryptophan Escherichia coli
[Expand this list w/ BRENDA]
Aryl hydrocarbon receptor (full agonist)
Intestinal L cells (GLP-1 secretagogue)
•Human liver enzymes (substrate)
•Promotes host-microbe homeostasis at mucosa
•Influences host metabolism via GLP-1's visceral effects
•Metabolized into indoxyl sulfate in the liver
[1][6][7]
3-Indolepropionic acid Tryptophan Clostridium sporogenes [1]
Indole-3-aldehyde Tryptophan Lactobacillus spp.
(L. reuteri in particular)
Aryl hydrocarbon receptor (full agonist) •Promotes host-microbe homeostasis at mucosa [1][6]
Indoxyl sulfate Tryptophan
(Indole)
Homo sapiens sapiens Uremic toxin
•Induces renal and vascular dysfunction
•Associated with chronic kidney disease
•Associated with cardiovascular disease
[1][8]
[9][10]
p-Cresol Tyrosine Clostridium difficile
Clostridium scatologenes
•Human liver enzymes (substrate) •Metabolized into p-cresyl sulfate in the liver [1][11]
p-Cresyl sulfate Tyrosine
(p-Cresol)
Homo sapiens sapiens Uremic toxin
•Induces renal and vascular dysfunction
•Associated with chronic kidney disease
•Associated with cardiovascular disease
[1][8]
[9][10]
Trimethylamine Choline
Carnitine
[Expand this list w/ BRENDA] Trace amine-associated receptor 5 (full agonist)
•Other unidentified olfactory receptors (agonist)
•Liver FMO3 enzymes (enzyme substrate)
•Smells foul (fishy or ammoniacal)
•Excessive production causes fish odor syndrome
•Promotes kidney dysfunction and atherogenesis
via liver metabolism to trimethylamine N-oxide
[1][12]
[13][14]
Conjugated linoleic acid
Conjugated linolenic acid
Linoleic acid
α-Linolenic acid
Lachnospiraceae spp.
Lactobacillus spp.
Bifidobacteria spp.
Propionibacterium spp.
Faecalibacterium prausnitzii
[1]

 • named ref citations used in the table above that are currently included in the article lead or the diagram.[1][8][13][14]

Reflist

References

  1. ^ a b c d e f g h i j k l Zhang LS, Davies SS (April 2016). "Microbial metabolism of dietary components to bioactive metabolites: opportunities for new therapeutic interventions". Genome Med. 8 (1): 46. doi:10.1186/s13073-016-0296-x. PMC 4840492Freely accessible. PMID 27102537. Lactobacillus spp. convert tryptophan to indole-3-aldehyde (I3A) through unidentified enzymes [125]. Clostridium sporogenes convert tryptophan to IPA [6], likely via a tryptophan deaminase. ... IPA also potently scavenges hydroxyl radicals 
    Table 2: Microbial metabolites: their synthesis, mechanisms of action, and effects on health and disease
    Figure 1: Molecular mechanisms of action of indole and its metabolites on host physiology and disease
  2. ^ Louis P, Flint HJ (May 2009). "Diversity, metabolism and microbial ecology of butyrate-producing bacteria from the human large intestine". FEMS Microbiol. Lett. 294 (1): 1–8. doi:10.1111/j.1574-6968.2009.01514.x. PMID 19222573. 
  3. ^ Vital M, Howe AC, Tiedje JM (April 2014). "Revealing the bacterial butyrate synthesis pathways by analyzing (meta)genomic data". MBio. 5 (2): e00889. doi:10.1128/mBio.00889-14. PMC 3994512Freely accessible. PMID 24757212. 
  4. ^ "Butyric acid". IUPHAR. IUPHAR/BPS Guide to PHARMACOLOGY. Retrieved 23 May 2015. 
  5. ^ "butanoic acid, 4 and Sodium; butyrate". BindingDB. The Binding Database. Retrieved 23 May 2015. 
  6. ^ a b Romani L, Zelante T, Palmieri M, Napolioni V, Picciolini M, Velardi A, Aversa F, Puccetti P (March 2015). "The cross-talk between opportunistic fungi and the mammalian host via microbiota's metabolism". Semin Immunopathol. 37 (2): 163–171. doi:10.1007/s00281-014-0464-2. PMID 25404119. A variety of indole derivatives, which are generated through the catabolism of dietary trp by tryptophanase in commensal intestinal bacteria [78], also acts as endogenous ligands for AhR [79]. By adopting a “top-down strategy” to screen host/biofluids/tissues for component of microbial origin, a microbial trp metabolic pathway leading to the production of indole-3-aldehyde (IAld) has recently been identified that preserves immune physiology at mucosal surfaces while inducing anticandidal resistance via AhR [41]. Lactobacilli, Lactobacillus reuteri in particular, were expanded under conditions of unrestricted availability of trp, such as in settings of IDO1 deficiency or on supplemental trp feeding. Most importantly, the increased availability of intestinal trp not only selectively expanded specific lactobacilli populations but could also promote alternate pathways of trp degradation by the lactobacilli population being expanded [41]. Indeed, metabolomics revealed that, of the different putative metabolites, IAld was abundantly produced by L. reuteri in the gut in the presence of trp and was capable of activating ILC3 for IL-22 production via AhR. Much like probiotics, IAld fulfilled the requirement of protecting and maintaining mucosal integrity during fungal infections or chemical damage [41]. Thus, the AhR agonistic activity of IAld could be exploited to provide homeostasis and microbial symbiosis at mucosal surfaces. Commensal lactobacilli are greatly reduced by stress [80, 81], and in the neonatal period [82], as well as in bacterial vaginitis, clinical conditions in which the empirical use of lactobacilli as probiotics to prevent infection have long been recommended yet never until now been mechanistically explained. 
  7. ^ "tryptophanase". BRENDA. Technische Universität Braunschweig. Retrieved 2 July 2016. 
  8. ^ a b c Wikoff WR, Anfora AT, Liu J, Schultz PG, Lesley SA, Peters EC, Siuzdak G (2009). "Metabolomics analysis reveals large effects of gut microflora on mammalian blood metabolites". Proc. Natl. Acad. Sci. U.S.A. 106 (10): 3698–703. doi:10.1073/pnas.0812874106. PMC 2656143Freely accessible. PMID 19234110. Production of IPA was shown to be completely dependent on the presence of gut microflora and could be established by colonization with the bacterium Clostridium sporogenes. 
    IPA metabolism diagram
  9. ^ a b Lin CJ, Wu V, Wu PC, Wu CJ (July 2015). "Meta-Analysis of the Associations of p-Cresyl Sulfate (PCS) and Indoxyl Sulfate (IS) with Cardiovascular Events and All-Cause Mortality in Patients with Chronic Renal Failure". PLoS ONE. 10 (7): e0132589. doi:10.1371/journal.pone.0132589. PMC 4501756Freely accessible. PMID 26173073. 
  10. ^ a b Vanholder R, Schepers E, Pletinck A, Nagler EV, Glorieux G (September 2014). "The uremic toxicity of indoxyl sulfate and p-cresyl sulfate: a systematic review". J. Am. Soc. Nephrol. 25 (9): 1897–1907. doi:10.1681/ASN.2013101062. PMC 4147984Freely accessible. PMID 24812165. 
  11. ^ "4-hydroxyphenylacetate decarboxylase". BRENDA. Technische Universität Braunschweig. Retrieved 2 July 2016. 
  12. ^ Liberles SD (October 2015). "Trace amine-associated receptors: ligands, neural circuits, and behaviors". Curr. Opin. Neurobiol. 34: 1–7. doi:10.1016/j.conb.2015.01.001. PMID 25616211. 
  13. ^ a b Falony G, Vieira-Silva S, Raes J (2015). "Microbiology Meets Big Data: The Case of Gut Microbiota-Derived Trimethylamine". Annu. Rev. Microbiol. 69: 305–321. doi:10.1146/annurev-micro-091014-104422. PMID 26274026. we review literature on trimethylamine (TMA), a microbiota-generated metabolite linked to atherosclerosis development. 
  14. ^ a b Gaci N, Borrel G, Tottey W, O'Toole PW, Brugère JF (November 2014). "Archaea and the human gut: new beginning of an old story". World J. Gastroenterol. 20 (43): 16062–16078. doi:10.3748/wjg.v20.i43.16062. PMC 4239492Freely accessible. PMID 25473158. Trimethylamine is exclusively a microbiota-derived product of nutrients (lecithin, choline, TMAO, L-carnitine) from normal diet, from which seems originate two diseases, trimethylaminuria (or Fish-Odor Syndrome) and cardiovascular disease through the proatherogenic property of its oxidized liver-derived form. 

uterus sub section[edit]

[1] might be good to add to above sub section (I have access to full article if needed)--Ozzie10aaaa (talk) 22:29, 27 June 2016 (UTC)

Thank you for your suggested source. I can get on with adding content and references and have some peace. Best Regards,Barbara (WVS) (talk) 03:42, 1 July 2016 (UTC)
I think I know what you mean--Ozzie10aaaa (talk) 11:34, 11 July 2016 (UTC)