Effect of cathepsin L activation on trichloroethylene-induced skin allergy in mice / 中国职业医学

ABSTRACT

OBJECTIVE: To observe the expression of cathepsin L( CTSL) on the skin of trichloroethylene( TCE)-sensitized mice,and explore the mechanism of CTSL in TCE-induced immunological skin damage. METHODS: The specific pathogen free female BALB/c mice were randomly divided into blank control group( n = 5),solvent control group( n = 5),TCE group( n = 15) and inhibitor group( n = 15). Skin sensitization experiments were performed according to the maximum guinea pig test method. The TCE group and inhibitor group were divided into sensitized subgroups and non-sensitized subgroups according to skin sensitization results. The skin tissues were taken 72 hours after the last TCE challenge.Hematoxylin-eosin staining was used to observe the pathological structure of skin tissues and measured the thickness of epidermis. The level of Ctsl mRNA was examined by real-time quantitative polymerase chain reaction,and the expression of CTSL, interleukin( IL)-6 and IL-17 were studied by immunohistochemical staining technique. RESULTS: The sensitization rate of TCE group and inhibitor group were 40. 0%(6/15) and 33. 3%(5/15) respectively. There was no statistical difference in the sensitization rate between the two groups( P > 0. 05). The thickness of epidermis and relative expression of Ctsl mRNA,CTSL,IL-6 and IL-17 in TCE sensitized subgroup and inhibitor sensitized subgroup were higher than that in blank control group,solvent control group,TCE non-sensitized subgroup and inhibitor non-sensitized subgroup(P < 0. 05). The above-mentioned indexes were higher in TCE sensitized subgroup than that in inhibitor sensitized subgroup( P < 0. 05). The relative expression of Ctsl mRNA,CTSL,IL-6 and IL-17 in skin of TCE sensitized subgroup were positively correlated between any two indexes( P < 0. 05). CONCLUSION: CTSL activation may play an important role in immunological skin damage of TCE-sensitized mice,which may be related to the promotion of IL-6 and IL-17 release.