2011 Fiscal Year Final Research Report

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

Research Project

Project/Area Number	21591301
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Single-year Grants
Section	一般
Research Field	Infectious disease medicine
Research Institution	Tokyo Medical University
Principal Investigator	MATSUMOTO Tetsuya 東京医科大学, 医学部, 教授 (10256688)
Project Period (FY)	2009 – 2011
Keywords	腸管免疫 / 腸内細菌 / bacterial translocation / 免疫不全
Research Abstract	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.