Changes Of Interleukin-17A And Interleukin-22 In The Lung Of Cigarette Smoke Exposed Mice And The Effect Of N-acetylcysteine

Objective To investigate the changes of interleukin-17A(IL-17A) and interleukin-22(IL-22) in the lung of cigarette smoke-exposed mice and effect of smoking cessation and N-acetylcysteine(NAC) treatment.Methods Male BALB/c mice were randomly assigned into control group, cigarette smoke-exposing group, smoking cessation group, and NAC treating group. Mice in all experimental groups were exposed to cigarette smoking for 20 weeks. After 20 weeks of exposure,1 mice of each group was killed to check emphysematous pathological change, then the mice in the control group and smoke-exposing group were executed. Bronchoalveolar lavage fluid(BALF) and lung tissue samples were collected. The mice in smoking cessation group were no longer treated with cigarette smoking. Mice in NAC group were treated with NAC. Every four weeks, a certain number of mice in the later two groups were sacrificed and BALF, lung tissue samples were collected. H&E staining was used to observe the pathologic changes of the lung. Leucocytes in BALF were counted in a blind method. ELISA was used to measure the levels of IL-17A and IL-22.Results Emphysematous change was found in the lung of cigarette smoke-exposed mice. No obvious mitigation of emphysematous changes in mice ceased cigarette smoking and NAC-treated ones. The number of leucocytes in BALF increased dramatically in cigarette smoke-exposed mice. Except for the mice with 4 weeks of smoking cessation, mice of the other intervention groups showed a statistic leucocyte counts decline, yet remained different from that of the control. Compared with control group, levels of IL-17A elevated in pulmonary homogenates and BALF after cigarette smoke exposure (P<0.05). Compared to smoke-exposure group, the level of IL-17A in smoking cessation for 4 weeks group showed no decline. After 8 weeks of smoking cessation, IL-17A levels in both pulmonary homogenates and BALF decreased statistical significantly. After 12 weeks of smoking cessation, IL-17A descended to the level of the control group. Compared to smoke-exposure group, each group in NAC intervention demonstrated statistical decline. When compared to smoking cessation for 4 weeks, IL-17A in NAC intervention for 4 weeks showed obvious decrease to control level(P<0.05). Compared to the control group, level of IL-22 in smoke-exposure group obviously rose; In smoking cessation for 4 weeks group, the IL-22 in pulmonary homogenates and BALF did not change statistically; In smoking cessation for 8 weeks group, IL-22 in BALF showed remarkable decline; After smoking cessation for 12 weeks, IL-22 in both pulmonary homogenates and BALF dramatically decreased, even to the control level. Compared with smoke-exposure group, in pulmonary homogenates and BALF, level of IL-22 of NAC gavage groups declined, even to a level of the control group in NAC intervention for 12 weeks. In NAC intervention for 4 weeks group, the level of IL-22 in pulmonary homogenates and BALF showed obvious decrease compared to smoking cessation for 4 weeks group. IL-22 to IL-17A ratio demonstrated an descent tendency.Conclusion IL-17A and IL-22 is implicated in the chronic inflammatory changes of lung in mice exposed to cigarette smoke. Smoking cessation and NAC intervention could attenuated cigarette smoke-induced lung inflammation, which might be related to IL-17A and IL-22.