Intestinal epithelium, intraepithelial lymphocytes and the gut microbiota-Key players in the pathogenesis of celiac disease

Celiac disease(CD) is a chronic immune-mediated disorder triggered by the ingestion of gluten in genetically predisposed individuals. Before activating the immune system, gluten peptides are transferred by the epithelial barrier to the mucosal lamina propria, where they are deamidated by intestinal tissue transglutaminase 2. As a result, they strongly bind to human leucocyte antigens(HLAs), especially HLA-DQ2 and HLA-DQ8, expressed on antigen-presenting cells. This induces an inflammatory response, which results in small bowel enteropathy. Although gluten is the main external trigger activating both innate and adaptive(specific) immunity, its presence in the intestinal lumen does not fully explain CD pathogenesis. It has been hypothesized that an early disruption of the gut barrier in genetically susceptible individuals, which would result in an increased intestinal permeability, could precede the onset of gluten-induced immune events. The intestinal barrier is a complex functional structure, whose functioning is dependent on intestinal microbiotahomeostasis, epithelial layer integrity, and the gutassociated lymphoid tissue with its intraepithelial lymphocytes(IELs). The aim of this paper was to review the current literature and summarize the role of the gut microbiota, epithelial cells and their intercellular junctions, and IELs in CD development.

Colonization of germ-free mice with a mixture of three lactobacillus strains enhances the integrity of gut mucosa and ameliorates allergic sensitization

临床的试用和动物实验的增加的数字显示出细菌为过敏症预防正在答应工具的那 probiotic。这里，我们在过敏促进感受性上分析了三选择乳杆菌紧张的 immunomodulatory 性质和他们的混合的影响赌 1 用一只 gnotobiotic 老鼠建模的 v。我们显示出那乳杆菌(L.) rhamnosus LOCK0900， L。rhamnosus LOCK0908 和 L。casei LOCK0919 经由像使用费的受体被认出 2 (TLR2 ) 并且核苷酸绑定 oligomerization 包含域的蛋白质 2 (NOD2 ) 受体并且刺激骨头在种类依赖者和紧张依赖者礼貌生产 cytokines 的导出髓的树枝状的房间。殖民无菌(GF ) 有所有三紧张(Lmix ) 的混合物的鼠标由加强 enterocytes 的顶端的 junctional 建筑群并且恢复延续到终端网的微细丝的结构改进了肠的障碍。与 Lmix 开拓殖民地于并且敏化 1 变应原到赌注 v 的老鼠显著地象一个增加的转变生长因素(TGF ) 一样在 sera 和肠的 lavages 显示出变应原特定的 IgE， IgG1 和 IgG2a 和提高的全部的 IgA 水平的底层 -&#x003B2；与敏化的 GF 老鼠相比铺平。从开拓殖民地于 Lmix 的老鼠的 Splenocytes 和 mesenteric 淋巴节点房间显示出 TGF-&#x003B2 的重要 upregulation；在以后在有赌注 v 的 vitro 刺激 1。我们的结果证明 Lmix 殖民改进了内脏对赌注 v 的上皮的障碍和减少的过敏促进感受性 1。而且，这些调查结果被传播和能分泌的 IgA 和规章的 cytokine TGF-&#x003B2 的增加的生产伴随；。因此，三乳杆菌紧张的这混合物在人在增加的内脏渗透和过敏症的发作的预防为使用显示出潜力。