Background: Allergic asthma is a chronic inflammatory airway disease characterized by eosinophilic inflammation, mucus hypersecretion, and type 2 immune responses. However, the role of CD300c in allergic airway inflammation remains unclear.

Objective: This study investigated the role of CD300c in OVA-induced allergic asthma using CD300c-deficient mice.

Methods: Wild-type (WT), CD300c knockout (KO), and CD300c full knockout (FKO) mice were sensitized and challenged with OVA. Airway inflammation was evaluated by bronchoalveolar lavage fluid (BALF) differential cell analysis, H&E and PAS staining, and RT-qPCR analysis of inflammation-related genes.

Results: Compared with WT mice, CD300c-deficient mice showed a trend toward reduced inflammatory cell infiltration in BALF following OVA challenge. Histological analysis also indicated decreased inflammatory cell infiltration, goblet cell hyperplasia, and mucus production. Similar trends were observed in inflammation-related gene expression.

Conclusions: CD300c deficiency tended to attenuate OVA-induced airway inflammation, goblet cell hyperplasia, and mucus production. These findings suggest that CD300c may contribute to allergic airway inflammation.