王洪武, 邓超, 蔡兴俊. 烟草烟雾暴露对哮喘小鼠气道炎症的影响[J]. 环境与职业医学, 2019, 36(8): 773-776. DOI: 10.13213/j.cnki.jeom.2019.19113
引用本文: 王洪武, 邓超, 蔡兴俊. 烟草烟雾暴露对哮喘小鼠气道炎症的影响[J]. 环境与职业医学, 2019, 36(8): 773-776. DOI: 10.13213/j.cnki.jeom.2019.19113
WANG Hong-wu, DENG Chao, CAI Xing-jun. Effects of tobacco smoke exposure on airway inflammation in asthmatic mice[J]. Journal of Environmental and Occupational Medicine, 2019, 36(8): 773-776. DOI: 10.13213/j.cnki.jeom.2019.19113
Citation: WANG Hong-wu, DENG Chao, CAI Xing-jun. Effects of tobacco smoke exposure on airway inflammation in asthmatic mice[J]. Journal of Environmental and Occupational Medicine, 2019, 36(8): 773-776. DOI: 10.13213/j.cnki.jeom.2019.19113

烟草烟雾暴露对哮喘小鼠气道炎症的影响

Effects of tobacco smoke exposure on airway inflammation in asthmatic mice

  • 摘要: 背景 吸烟或曾经吸烟患者哮喘发病及严重程度与未吸烟哮喘患者明显不同,表现为激素依赖或激素抵抗,烟草烟雾暴露是导致难治性哮喘的重要原因。

    目的 探讨烟草烟雾暴露后支气管哮喘模型小鼠气道炎性细胞及相关细胞因子的变化。

    方法 将40只小鼠随机分为4组,包括正常对照组、哮喘组、烟草烟雾暴露组、烟草烟雾暴露+哮喘组,每组各10只。哮喘组小鼠第0、14天腹腔注射0.2 mL致敏液(含OVA 100 μg、氢氧化铝凝胶400 μg),第24天用1% OVA溶液10 mL雾化激发,每天30 min,连续28 d。正常对照组及烟草烟雾暴露组小鼠以等量生理盐水替代致敏液及雾化液,烟草烟雾暴露组小鼠在每次雾化吸入后30 min被动烟草烟雾静式吸入暴露1次,每次10支,持续1 h。烟草烟雾暴露+哮喘组小鼠按哮喘组方法致敏和雾化激发,并按烟草烟雾暴露组处理方法吸入烟草烟雾。28 d后采集支气管肺泡灌洗液(BALF),用ELISA方法检测白介素(IL)-1、IL-6、IL-8、IL-17A、IL-17F浓度;测定BALF中白细胞(WBC)、嗜酸性粒细胞(EOS)及中性粒细胞(NEU)计数。

    结果 哮喘组、烟草烟雾暴露+哮喘组BALF中WBC、EOS、NEU均高于正常对照组、烟草烟雾暴露组,差异均有统计学意义(P < 0.05)。烟草烟雾暴露+哮喘组BALF中WBC、NEU计数分别为(20.65±1.90)×104/L、(16.33±1.54)×104/L高于哮喘组(16.12±1.53)×104/L、(3.57±0.75)×104/L,EOS计数(4.68±0.88)×104/L低于哮喘组(12.54±1.12)×104/L,差异均有统计学意义(P < 0.05)。烟草烟雾暴露+哮喘组BALF中IL-1、IL-6、IL-8、IL-17A和IL-17F水平分别为(28.93±5.91)、(70.46±7.18)、(188.64±10.43)、(146.77±9.07)、(90.87±7.52)ng/L均高于哮喘组(22.69±3.35)、(53.57±6.42)、(126.17±8.95)、(104.35±6.92)、(73.71±4.66)ng/L及烟草烟雾暴露组(11.37±2.32)、(23.38±4.75)、(88.13±7.12)、(76.12±6.88)、(43.90±4.18)ng/L,差异均有统计学意义(P < 0.05)。

    结论 烟草烟雾暴露加重哮喘气道炎症,炎性细胞以中性粒细胞浸润为主,气道炎症相关细胞因子释放增加。

     

    Abstract: Background The incidence and severity of asthma in smokers or former smokers are significantly different from those in non-smokers, usually hormonal dependence or hormonal resistance. Tobacco smoke exposure is an important cause of refractory asthma.

    Objectve This experiment is designed to investgate the changes of airway inflammatory cells and related cytokines in mice with bronchial asthma afer exposure to tobacco smoke.

    Methods Forty mice were randomly divided into normal control group, asthma group, tobacco smoke exposure group, and tobacco smoke exposure+asthma group, with 10 mice in each group. The mice in the asthma group were intraperitoneally injected with 0.2 mL sensitizing solution (including OVA 100 μg and aluminum hydroxide gel 400 μg) on day 0 and day 14, and atomized with 10 mL 1% OVA soluton on day 24, 30 min per day for consecutve 28 days. The mice in the normal control group and the tobacco smoke exposure group were given the same amount of normal saline instead of sensitizing fluid and atomizing fluid. The mice in the tobacco smoke exposure group were exposed to passive tobacco smoke by statc inhalaton 30 min afer each atomized inhalaton, each tme with 10 commercial cigaretes for 1 h. The mice in the tobacco smoke exposure+asthma group were sensitzed and atomized as the asthma group, and inhaled tobacco smoke as the tobacco smoke exposure group. Afer 28 days, bronchoalveolar lavage fluid (BALF) was collected to detect the concentratons of interleukin (IL)-1, IL-6, IL-8, IL-17A, and IL-17F by ELISA and count white blood cells (WBC), eosinophils (EOS), and neutrophils (NEU).

    Results The WBC, EOS and NEU counts in BALF of the asthma group and the tobacco smoke exposure + asthma group were higher than those of the control group and the tobacco smoke exposure group, respectively (P < 0.05). The WBC and NEU counts in BALF of the tobacco smoke exposure+asthma group(20.65±1.90)×104/L, (16.33±1.54)×104/L were higher than those of the asthma group(16.12±1.53)×104/L, (3.57±0.75)×104/L, and the EOS count(4.68±0.88)×104/L was lower than that of the asthma group(12.54±1.12)×104/L, respectvely (P < 0.05). The levels of IL-1, IL-6, IL-8, IL-17A, and IL-17F in BALF of the tobacco smoke exposure+asthma group(28.93±5.91), (70.46±7.18), (188.64±10.43), (146.77±9.07), and (90.87±7.52) ng/L were higher than those in the asthma group(22.69±3.35), (53.57±6.42), (126.17±8.95), (104.35±6.92), and (73.71±4.66) ng/L and the tobacco smoke exposure group(11.37±2.32), (23.38±4.75), (88.13±7.12), (76.12±6.88), and (43.90±4.18) ng/L, respectvely (P < 0.05).

    Conclusion The airway inflammaton in asthma is aggravated by tobacco smoke exposure, the inflammatory cells are mainly infltrated by neutrophils, and the release of related cytokines is increased.

     

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