Expression of toll-like receptor 2 (TLR2), TLR4, and CD14 in biopsy samples of patients with inflammatory bowel diseases: Upregulated expression of TLR2 in terminal ileum of patients with ulcerative colitis
Expression of toll-like receptor 2 (TLR2), TLR4, and CD14 in biopsy samples of patients with inflammatory bowel diseases: Upregulated expression of TLR2 in terminal ileum of patients with ulcerative colitis
复制标题
DOI：
10.1369/jhc.7a7303.2007
复制
发表时间：
2008-03-01
影响因子：
3.2
通讯作者：
Tlaskalova-Hogenova, Helena
中科院分区：
文献类型：
--
作者：
Frolova, Lenka;Drastich, Pavel;Tlaskalova-Hogenova, Helena
肠道对细菌I型菌群的先天性和适应性免疫应答失调被认为参与了炎症性肠病（IBD）的发病机制。我们研究了Toll样受体2（TLR2），TLR4，和他们的跨膜辅助受体CD14在IBD患者和对照组的非炎症肠粘膜活检样本的表达。通过结肠镜检查从克罗恩病（CD）、溃疡性结肠炎（UC）患者和对照组获得小肠和结肠样品。使用TLR2、TLR4和CD14特异性多克隆和单克隆抗体对冷冻切片进行免疫组织化学分析，结果显示与对照组相比，非活动性和活动性UC患者回肠末端TLR2表达显著增加。与对照组相比，缓解期UC患者的回肠末端和直肠以及活动期CD患者的回肠末端TLR4表达显著上调。CD 14表达在CID缓解期和活动期患者的回肠末端、UC缓解期和活动期患者的盲肠以及UC活动期患者的直肠中上调。因此，TLR2、TLR4和CD14在肠粘膜不同部位的表达失调可能在IBD发病机制中至关重要。
Dysregulation of innate and adaptive intestinal immune responses to bacteria I microbiota is supposed to be involved in pathogenetic mechanisms of inflammatory bowel diseases (IBDs). We investigated expression of Toll-like receptor 2 (TLR2), TLR4, and their transmembrane coreceptor CD14 in biopsy samples from patients with IBD and in non-inflamed gut mucosa from controls. Small intestine and colon samples were obtained by colonoscopy from patients with Crohn's disease (CD), ulcerative colitis (UC), and controls. Immunohistochemical analysis of cryostat sections using polyclonal and monoclonal antibodies specific for TLR2, TLR4, and CD14 showed a significant increase in TLR2 expression in the terminal ileum of patients with inactive and active UC against controls. Significant upregulation of TLR4 expression relative to controls was found in the terminal ileum and rectum of UC patients in remission and in the terminal ileum of CD patients with active disease. CD14 expression was upregulated in the terminal ileum of CID patients in remission and with active disease, in the cecum of UC patients in remission and with active disease, and in rectum of UC patients with active disease. Hence, dysregulation of TLR2, TLR4, and CD14 expression in different parts of the intestinal mucosa may be crucial in IBD pathogenesis.