TLR5 expression in the small intestine depends on the adaptors MyD88 and TRIF, but is independent of the enteric microbiota.
In our recent article Hörmann and coworkers have reported a role for epithelial cell-intrinsic TLR2 signaling for proliferation and renewal of the small intestinal epithelium. In this study, MyD88 and TRIF expression in the small intestine were affected by gut microbiota. Here, we report that in contrast to TLR2 and its co-receptor TLR1, TLR5 transcripts are not changed by presence of gut microbiota nor regulated through TLR2 or TLR4. Similar to TLR2 also TLR5 depends on MyD88 and TRIF adaptors. Our results indicate that TLR adaptor molecules could be determinants of TLR expression in the small intestine.
a Center for Thrombosis and Hemostasis (CTH); University Medical Center Mainz; Junior Group Translational Research in Thrombosis and Hemostasis ; Mainz , Germany.
Inês
I
Brandão
Nives
N
Hörmann
Sven
S
Jäckel
Christoph
C
Reinhardt
D033942:Adaptor Proteins, Vesicular Transport / Q000378:metabolism*; D000069196:Gastrointestinal Microbiome / Q000276:immunology*; D015870:Gene Expression; D006801:Humans; D007421:Intestine, Small / Q000276:immunology* / Q000382:microbiology*; D064307:Microbiota / Q000276:immunology*; D008954:Models, Biological; D053594:Myeloid Differentiation Factor 88 / Q000378:metabolism*; D051198:Toll-Like Receptor 5 / Q000096:biosynthesis*
D033942:Adaptor Proteins, Vesicular Transport; C507779:MYD88 protein, human; D053594:Myeloid Differentiation Factor 88; C470409:TICAM1 protein, human; C495346:TLR5 protein, human; D051198:Toll-Like Receptor 5
MyD88; TLR2; TLR5; TOLLIP; TRIF; germ-free; gut microbiota; small intestine