Panettieri Reynold A
Pulmonary, Allergy and Critical Care Division, University of Pennsylvania Medical Center, 421 Curie Boulevard, 805 BRB II/III, Philadelphia, Pennsylvania, PA 19104-6160, USA.
Respir Physiol Neurobiol. 2003 Sep 16;137(2-3):277-93. doi: 10.1016/s1569-9048(03)00153-8.
Although the pathogenesis of asthma remains unclear, substantial progress has been made over the past decades in the characterization of airway inflammation as a pathogenetic mechanism in asthma. New evidence suggests that airway smooth muscle (ASM), the most important cell modulating bronchomotor tone, plays an important immunomodulatory role in the orchestration and perpetuation of airway inflammation. Evidence now suggests that the signaling pathways that modulate leukocyte function may be disparate from those found in resident effector cells such as ASM, fibroblasts and epithelial cells. Further investigation and understanding of the critical signaling pathways that modulate ASM cell release, secretion of chemokines/cytokines and expression of cell adhesion molecules (CAMs) may offer new therapeutic approaches in the treatment of asthma.
尽管哮喘的发病机制尚不清楚,但在过去几十年里,将气道炎症作为哮喘发病机制的特征描述方面已取得了重大进展。新证据表明,气道平滑肌(ASM)是调节支气管运动张力的最重要细胞,在气道炎症的协调和持续存在中发挥着重要的免疫调节作用。现在有证据表明,调节白细胞功能的信号通路可能与在诸如ASM、成纤维细胞和上皮细胞等驻留效应细胞中发现的信号通路不同。对调节ASM细胞释放、趋化因子/细胞因子分泌以及细胞粘附分子(CAMs)表达的关键信号通路进行进一步研究和了解,可能为哮喘治疗提供新的治疗方法。