O040 A novel role of Dectin-1 signaling in promoting intestinal inflammation

摘要: Introduction Dectin-1, which was first reported as a dentritic cell-specific type II C-type lectin family member, is the receptor for β-1,3 or −1,6-linked glucans (β-glucans), an important cell wall components of fungi and yeasts. Dysregulated response mucosal immune system toward intraluminal bacteria results in human inflammatory bowel disease (IBD). Beta-glucan thought to promote immunity intestines, but roles Dectin-1 are still unknown. Methods To investigate potential role development IBD, we administrated Decint-1 deficient ( clec7a −/− ) mice with dextran sulfate sodium (DSS) induce acute ulcerative colitis found that were significantly resistant DSS-induced compared wild-type (WT) mice, associated lower production TNF-α reduced numbers neutrophils macrophages lamina propria colon. Results Pre-treatment dectin-1 antagonist ligand Laminarin could suppress intestinal inflammation induced by DSS. Metagenome analysis using bacterial 16s rRNA genes revealed change microflora small intestine colon WT administration SPF condition germ-free also showed colitis. Conclusion These new findings identify novel factor promotion directly inducing proinflammatory cytokines regulating balance microbiota. Blockade signaling suggests therapeutic strategies diseases.