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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