Activation of intestinal mucosal immunization via probiotic strain with the mechanism of Cd1d and NKT cell

我们研究了控制肠道细菌定植的宿主机制。在特定病原体下。无菌或无菌条件下，胃内给予铜绿假单胞菌、E.大肠杆菌，金黄色葡萄球菌，或加氏乳杆菌导致增加小肠定植和细菌易位的小鼠缺乏Cd 1d，与野生型小鼠相比。相反，用α-半乳糖神经酰胺激活Cd 1d限制性T细胞（NKT细胞）导致相同细菌菌株的肠道定植减少。体外数据表明，NKT细胞显示出诱导溶菌酶从肠隐窝释放。这些数据支持Cd 1d通过包括潘氏细胞功能控制在内的机制在调节肠道定植中的作用。

We studied the host mechanisms involved in controlling intestinal colonization with commensal bacteria. Under specific pathogen. free or germ-free conditions, intragastric administration of Pseudomonas aeruginosa, E. coli, Staphylococcus aureus, or Lactobacillus gasseri resulted in increased colonization of the small intestine and bacterial translocation in mice lacking Cd1d, compared with wild type mice. In contrast, activation of Cd1d-restricted T cells(NKT cells) withα-galactosylceramide caused diminished intestinal colonization with the same bacterial strains. In vitro data suggest that NKT cells were shown to induce the release of lysozyme from intestinal crypts. These data support a role for Cd1d in regulating intestinal colonization through mechanisms that include the control of Paneth cell function.