Tulic Meri K, Hamid Qutayba
Meakins-Christie Laboratories, McGill University, Montreal, Quebec, Canada.
Semin Respir Crit Care Med. 2002 Aug;23(4):347-59. doi: 10.1055/s-2002-34330.
Accumulating patholological and physiological evidence in the last few years suggests that the airway inflammation and remodeling that characterize asthma occur not only in the central airways but extend to the distal lung and the lung parenchyma. The distal airways are capable of producing T-helper (Th)2 cytokines as well as chemokines, and more recently, they have been recognized as a predominant site of airflow obstruction in asthmatics. A similar TH2-type cytokine profile and infiltration of inflammatory cells has also been reported in the lung parenchyma. The inflammation at this distal site has been described as more severe when compared with the large airway inflammation, and evidence of remodeling in the lung periphery is emerging. Recognition of asthma as a disease of the entire respiratory tract has an important clinical significance highlighting the need also to consider the distal lung as a target in any therapeutic strategy for effective treatment of this disease.
过去几年中不断积累的病理和生理证据表明，作为哮喘特征的气道炎症和重塑不仅发生在中央气道，还会延伸至远端肺组织和肺实质。远端气道能够产生辅助性T（Th）2细胞因子以及趋化因子，并且最近它们已被认为是哮喘患者气流阻塞的主要部位。在肺实质中也报道了类似的Th2型细胞因子谱和炎症细胞浸润。与大气道炎症相比，该远端部位的炎症被描述为更严重，并且肺周边重塑的证据正在出现。将哮喘视为一种全呼吸道疾病具有重要的临床意义，这突出表明在任何有效治疗该疾病的治疗策略中，也需要将远端肺组织作为一个靶点来考虑。
