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

我们研究了共生菌控制肠道定植的宿主机制。在特定病原体的作用下。在无菌或无菌条件下，与野生型小鼠相比，灌胃给予铜绿假单胞菌、大肠杆菌、金黄色葡萄球菌或加瑟氏乳杆菌可导致缺乏CD1d的小鼠小肠定植和细菌移位增加。相反，用α-半乳糖神经酰胺激活CD1d限制性T细胞(NKT细胞)会减少对相同菌株的肠道定植。体外数据表明，NKT细胞可以诱导肠道隐窝释放溶菌酶。这些数据支持CD1d通过包括控制Paneth细胞功能在内的机制来调节肠道定植。

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.