Nadel J A
J Allergy Clin Immunol. 1984 May;73(5 Pt 2):651-3. doi: 10.1016/0091-6749(84)90299-9.
Extreme sensitivity of airways to multiple stimuli characterizes asthma. Airway hyperresponsiveness can be produced experimentally in otherwise healthy subjects or animals by inflammatory damage (e.g., induced by respiratory viruses or by inhaled oxidants). Evidence is presented that cell-to-cell interactions play an important role in experimental hyperreactivity and that similar inflammatory cascades may play a similar role in clinical asthma. Although the importance of epithelial cells and neutrophils has been identified in the present studies, other inflammatory mechanisms (e.g., sensory nerve release of substance P, epithelial mast cells, eosinophils) may also play key roles. In exercise-induced bronchospasm, the stimulus (e.g., cooling or drying) must affect a cell (e.g., one near the epithelial surface) by decreasing temperature or by increasing osmolality. This signal may cause mediator release and a subsequent cascade, leading to contraction of smooth muscle. Environmental irritants (e.g., ozone) inhaled during exercise may potentiate these effects by producing further inflammation.
气道对多种刺激的极度敏感是哮喘的特征。在原本健康的受试者或动物中，炎症损伤（如由呼吸道病毒或吸入氧化剂诱导）可通过实验产生气道高反应性。有证据表明，细胞间相互作用在实验性高反应性中起重要作用，且类似的炎症级联反应可能在临床哮喘中起类似作用。尽管在目前的研究中已确定上皮细胞和中性粒细胞的重要性，但其他炎症机制（如感觉神经释放P物质、上皮肥大细胞、嗜酸性粒细胞）也可能起关键作用。在运动诱发性支气管痉挛中，刺激因素（如冷却或干燥）必须通过降低温度或增加渗透压来影响细胞（如上皮表面附近的细胞）。该信号可能导致介质释放及随后的级联反应，进而导致平滑肌收缩。运动期间吸入的环境刺激物（如臭氧）可能通过引发进一步炎症来增强这些效应。
