Giardia ⇒ Blastocystis {10001411}

Shared Reference Notes

• [1.1] [#Spondyloarthritis] 
  - SpA patients colonized by Blastocystis showed significant increases in the phylum Pseudomonadota, class #Gammaproteobacteria, family #Succinivibrionaceae, and genus #Succinivibrio.
• [1.2] [#Inflamatory bowel disease] 
  - infections with parasites like #Strongyloides stercoralis and Blastocystis have been shown to mimic the symptoms of IBD, highlighting the intricate relationship between parasites and the pathogenesis of these diseases.
• [1.3] [#Indole-3-acetic acid] 
  - Blastocystis ST4 expresses the gene product of #Acetaldehyde dehydrogenase - This specific gene product potentially plays a role in the degradation of I3AA to IAA.
• [#Indole-3-acetaldehyde] - 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.
• [#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.

References Notes