小肠中的Toll样受体5（TLR5）表达依赖于衔接蛋白髓样分化因子88（MyD88）和TIR结构域衔接蛋白诱导干扰素β（TRIF），但不依赖于肠道微生物群。
TLR5 expression in the small intestine depends on the adaptors MyD88 and TRIF, but is independent of the enteric microbiota.
作者信息
Brandão Inês, Hörmann Nives, Jäckel Sven, Reinhardt Christoph
机构信息
a Center for Thrombosis and Hemostasis (CTH); University Medical Center Mainz; Junior Group Translational Research in Thrombosis and Hemostasis ; Mainz , Germany.
出版信息
Gut Microbes. 2015;6(3):202-6. doi: 10.1080/19490976.2015.1034417. Epub 2015 Apr 29.
Abstract
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.
摘要
在我们最近的文章中，霍尔曼及其同事报道了上皮细胞内源性Toll样受体2（TLR2）信号传导在小肠上皮细胞增殖和更新中的作用。在这项研究中，小肠中髓样分化因子88（MyD88）和TIR结构域衔接蛋白诱导干扰素β（TRIF）的表达受肠道微生物群影响。在此，我们报道，与TLR2及其共受体TLR1不同，Toll样受体5（TLR5）转录本不会因肠道微生物群的存在而改变，也不受TLR2或Toll样受体4（TLR4）调控。与TLR2相似，TLR5也依赖MyD88和TRIF衔接蛋白。我们的结果表明，Toll样受体衔接分子可能是小肠中Toll样受体表达的决定因素。
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