Melgert Barbro N, Postma Dirkje S, Geerlings Marie, Luinge Marjan A, Klok Pieter A, van der Strate Barry W A, Kerstjens Huib A M, Timens Wim, Hylkema Machteld N
Department of Pathology and Laboratory Medicine, University Hospital Groningen, P.O. Box 30.001, 9700 RB, Groningen, The Netherlands.
Am J Respir Cell Mol Biol. 2004 Jun;30(6):880-5. doi: 10.1165/rcmb.2003-0178OC. Epub 2004 Jan 12.
Little is known about effects of smoking on airway inflammation in asthma. We tested the hypothesis that smoking enhances established airway inflammation in a mouse model of allergic asthma. C57Bl/6j mice were sensitized to ovalbumin (OVA) and challenged with OVA (OVA-mice) or sham-sensitized to phosphate-buffered saline (PBS) and challenged with PBS aerosols (PBS-mice) for 7 wk. At 4 wk, mice were additionally exposed to air (nonsmoking controls) or mainstream smoke for 3 wk. Using whole body plethysmography, we found OVA-induced bronchoconstriction to be significantly inhibited in smoking OVA-mice as compared with nonsmoking OVA-mice (1 +/- 2% increase versus 22 +/- 6% increase in enhanced pause, respectively). Smoking did not change airway hyperresponsiveness (AHR) to methacholine in PBS-mice, yet significantly attenuated AHR in OVA-mice 24 h after OVA challenge as compared with nonsmoking mice. This was accompanied by reduced eosinophil numbers in lung lavage fluid and tissue of smoking OVA-mice compared with nonsmoking OVA-mice. In contrast to our hypothesis, short-term smoking reduced responsiveness to OVA and methacholine in OVA-mice and decreased airway inflammation when compared with nonsmoking mice. This effect of smoking may be different for long-term smoking, in which remodeling effects of smoking can be expected to interrelate with remodeling changes caused by asthmatic disease.
关于吸烟对哮喘气道炎症的影响，人们所知甚少。我们验证了这样一个假说：在过敏性哮喘小鼠模型中，吸烟会加剧已有的气道炎症。将C57Bl/6j小鼠用卵清蛋白（OVA）致敏，并用OVA激发（OVA小鼠），或者用磷酸盐缓冲盐水（PBS）进行假致敏，并用PBS气雾剂激发（PBS小鼠），持续7周。在第4周时，小鼠额外暴露于空气（非吸烟对照组）或主流烟雾中3周。使用全身体积描记法，我们发现，与非吸烟的OVA小鼠相比，吸烟的OVA小鼠中OVA诱导的支气管收缩受到显著抑制（增强暂停分别增加1±2%和22±6%）。吸烟并未改变PBS小鼠对乙酰甲胆碱的气道高反应性（AHR），但与非吸烟小鼠相比，在OVA激发后24小时，吸烟的OVA小鼠的AHR显著减弱。与非吸烟的OVA小鼠相比，吸烟的OVA小鼠肺灌洗液和组织中的嗜酸性粒细胞数量减少。与我们的假说相反，与非吸烟小鼠相比，短期吸烟降低了OVA小鼠对OVA和乙酰甲胆碱的反应性，并减轻了气道炎症。吸烟的这种影响可能与长期吸烟不同，长期吸烟中，吸烟的重塑作用可能会与哮喘疾病引起的重塑变化相互关联。
