Objective：This study aims to explore the expression and potential mechanism of cell adhesion molecule L1-like protein（CHL1）in bronchial asthma. Methods：The clinical data and serum samples of 55 asthma patients and 18 healthy controls were collected，enzyme-linked immunosorbent assay was used to detect the expression of serum CHL1，then the correlation of CHL1 with pulmonary function related-indexor serum total immunoglobulin E（IgE）was analyzed. A mouse model of ovalbumin（OVA）-induced chronic allergic asthma was constructed，using immunohistochemistry to observe the localization and distribution pattern of CHL1 in lung tissue. The expression of CHL1 after stimulated by different cytokines in human bronchial epithelial cell line 16HBE was detected by real-time quantitative PCR and Western blot. Results：The level of serum CHL1 in the asthma group was higher than in the healthy control group［（7.497±3.274）ng/mL vs.（4.174±2.122）ng/mL，P < 0.000 1］，and is positively correlated with the level of serum total IgE（r=0.287，P=0.048）. CHL1 is mainly expressed in bronchial epithelial cells in mouse lung tissue，the expression level of CHL1 in asthma mice was higher than that in the control group. After stimulation of exogenous TGF-β at different times，the mRNA and protein levels of CHL1 were up-regulated. Conclusion：The expression of CHL1 is elevated in asthma，and this process may be related to TGF-β related signal pathways.