TLR Signaling-induced CD103-expressing Cells Protect Against Intestinal Inflammation
TLR Signaling-induced CD103-expressing Cells Protect Against Intestinal Inflammation
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TLR 信号传导诱导的 CD103 表达细胞可预防肠道炎症
DOI：
10.1097/mib.0000000000000292
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发表时间：
2015
影响因子：
4.9
通讯作者：
Frick JS
中科院分区：
文献类型：
--
作者：
Wittmann A;Bron PA;van Swam II;Kleerebezem M;Adam P;Gronbach K;Menz S;Flade I;Bender A;Schäfer A;Korkmaz AG;Parusel R;Autenrieth IB;Frick JS
背景：与健康对照相比，炎症性肠病患者的toll样受体（TLR）表达增加。然而，TLR信号在炎症性肠病中的作用尚不完全清楚。方法采用骨髓嵌合小鼠急性期炎症模型，探讨TLR2/4细胞类型信号诱导在预防肠道炎症中的重要作用及对肠道树突状细胞的影响。小鼠被喂食能够启动TLR2/4信号级联的野生型细菌或信号诱导能力受损的突变菌株。结果TLR2/4信号级联在骨髓嵌合小鼠上皮细胞中的诱导作用可引起炎症，而在造血细胞中的诱导作用则相反。此外，饲喂野生型细菌可以预防疾病；然而，不同的细菌信号诱导对固有层树突状细胞的激活没有影响。相比之下，功能性TLR2/4信号导致表达cd103的固有层和肠系膜淋巴结树突状细胞的频率增加，这能够改善疾病。结论TLR介导的疾病改善、cd103表达细胞的增加以及TLR信号诱导在造血细胞中的有益功能提示，炎症性肠病患者TLR表达的增加可能引起宿主的反调控，起到预防疾病的作用。
BackgroundToll-like receptor (TLR) expression in patients with inflammatory bowel disease is increased when compared with healthy controls. However, the impact of TLR signaling during inflammatory bowel disease is not fully understood.MethodsIn this study, we used a murine model of acute phase inflammation in bone marrow chimeric mice to investigate in which cell type TLR2/4 signal induction is important in preventing intestinal inflammation and how intestinal dendritic cells are influenced. Mice were either fed with wild-type bacteria, able to initiate the TLR2/4 signaling cascade, or with mutant strains with impaired signal induction capacity.ResultsThe induction of the TLR2/4 signal cascade in epithelial cells resulted in inflammation in bone marrow chimeric mice, whereas induction in hematopoietic cells had an opposed function. Furthermore, feeding of wild-type bacteria prevented disease; however, differing signal induction of bacteria had no effect on lamina propria dendritic cell activation. In contrast, functional TLR2/4 signals resulted in increased frequencies of CD103-expressing lamina propria and mesenteric lymph node dendritic cells, which were able to ameliorate disease.ConclusionsThe TLR-mediated amelioration of disease, the increase in CD103-expressing cells, and the beneficial function of TLR signal induction in hematopoietic cells indicate that the increased expression of TLRs in patients with inflammatory bowel disease might result in counterregulation of the host and serve in preventing disease.
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