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Lactobacillus spp. convert tryptophan to indole-3-aldehyde (I3A) through unidentified enzymes . Clostridium sporogenes convert tryptophan to IPA , 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
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A variety of indole derivatives, which are generated through the catabolism of dietary trp by tryptophanase in commensal intestinal bacteria , also acts as endogenous ligands for AhR . 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 . 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 . 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 . 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 , 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.
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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
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we review literature on trimethylamine (TMA), a microbiota-generated metabolite linked to atherosclerosis development.
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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.