Indole-3-acetaldehyde {90000647} Record Keys Parent:[ ] Definition:Indole-3-acetaldehyde Queue:[ ] Details Initialisation date:[ ] Specification: [ ]Source: [ ] Meta Information Structural Type:[ ] Functional Type:[ ] Function:[ ] Notes: [ ]Shared Reference Notes [1.1] - I3AA exhibits distinct inhibitory effects on regulatory T cells (Treg). I3AA alters the sensitivity of Treg cells to TGFβ signals, thereby impacting their function and ability to migrate to the gut. - #AHR-dependent mechanism, with I3AA acting as an antagonist of this intracellular receptor. - PD-1 expression positively correlates with #AHR activation by agonist ligands - #Blastocystis ST7 on the microbiome may lead to a reduction in the effectiveness of bacterial communities in clearing I3AA in the gut environment. - I3AA produced by #Blastocystis ST7 per se constitutes a pathogenic trait of this particular ST. - the preexisting and post-infection status of the microbiome in the context of processes targeting I3AA as a substrate for further metabolism might determine pathological outcome of this protist infection. -I3AA may serve as a substrate for the synthesis of #Indole-3-acetic acid (IAA) and indole-3-aldehyde (IAld). [#Inflamatory bowel disease] - protist #Blastocystis ST7 in a mouse model are associated with reduction of anti-inflammatory Treg cells and simultaneous expansion of pro-inflammatory Th17 responders. These alterations in CD4+ T cells depended on the #Tryptophan metabolite indole-3-acetaldehyde (I3AA) produced by this single-cell eukaryote. - I3AA reduced the Treg subset in vivo and iTreg development in vitro by modifying their sensing of TGFβ, concomitantly affecting recognition of self-flora antigens by conventional CD4+ T cells. - Parasite-derived I3AA also induces over-exuberant TCR signaling, manifested by increased CD69 expression and downregulation of co-inhibitor PD-1. [#Limosilactobacillus (Lactobacillus) reuteri] - Lactobacillus reuteri is known to be a common gut-dwelling strain that possesses the ability to produce (IAld) in the I3AA-dependet pathway. - This synthesis of IAld by L. reuteri results in #AHR-dependent #IL-22 production and gut protection from inflammation, indicating IAld as a beneficial bacterial-derived metabolite.References Notes[ ]
