Background: Inflammatory bowel disease (IBD) is characterized by chronic intestinal inflammation, epithelial barrier disruption, and dysregulated immune responses. Although CD300 family receptors are involved in immune regulation, the role of CD300c in intestinal inflammation remains unclear.

Objective: This study investigated the role of CD300c in intestinal inflammation using a dextran sulfate sodium (DSS)-induced colitis mouse model.

Methods: Wild-type (WT), Cd300c knockout (KO), and Cd300c full knockout (FKO) mice received 1.5% or 3% DSS in drinking water for 7 days, followed by normal drinking water during recovery. Disease severity was evaluated by body weight, stool consistency, rectal bleeding, colon length, spleen weight, histological analysis, and inflammatory gene expression.

Results: The 3% DSS treatment induced more pronounced body weight loss than 1.5% DSS, indicating greater severity. Most macroscopic parameters showed no significant differences among genotypes. However, significant differences in crypt density were observed among genotypes in the 3% DSS groups, suggesting genotype-dependent alterations in colonic tissue responses.

Conclusions: CD300c deficiency did not markedly alter the overall severity of DSS-induced colitis under these conditions but may influence specific histological responses to intestinal injury. Further histological, molecular, and immune cell analyses are required to clarify the role of CD300c in intestinal inflammation.