Abstract:Objective To investigate the pathological changes and the expression of IL-17 (IL-17) in different stages of chronic bronchiolitis obliterans model after heterotopic tracheal transplantation in rats.Methods Twenty-four cleangrade SD rats were selected, of which 6 were brown Norway (BN) and 18 were Lewis.Twelve Lewis rats were randomly selected into the control group, and the remaining six Lewis rats and six BN rats were included into the observation group.The BN rats in observation group provided trachea, Lewis rats received trachea;and the 12 Lewis rats in control group were both donor and receptor.The cartilage injury rate, lymphocyte count, incidence of bronchiolitis obliterans and the level of IL-17 were compared between the two groups.Results After transplantation, the incidence of bronchiolitis obliterans in the observation group was 100.00%, higher than that in the control group (0.00%), with statistically significant difference (P<0.05).There was no statistically significant difference in the cartilage damage rate between the two groups on the 7th day after transplantation (P>0.05).On the 14th and 28th days after transplantation, the cartilage damage rates in the observation group were higher than those in the control group, with statistically significant differences (P<0.05).After 7, 14 and 28 days of transplantation, the lymphocyte counts in the observation group were more than those in the control group, with statistically significant differences (P<0.05).There were no statistically significant differences in the levels of IL-17 between the two groups on the 7th and 14th days after transplantation (P>0.05).The level of IL-17 in the observation group was higher than that in the control group on the 28th day after transplantation,with statistically significant difference (P<0.05).Conclusion Through the establishment of the model of chronic rejection of ectopic trachea in rats, it is suggested that the level of IL-17 in rats increased after the transplantation of ectopic trachea, and the mechanism of occlusive inflammatory response induced by IL-17 should be further studied.
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