Gabbrielli S, Di Lollo S, Stanflin N, Romagnoli P
Division of Pneumology, U.S.L. 23, Arezzo, Italy.
Pathologica. 1994 Apr;86(2):157-60.
Considering the role proposed for myofibroblasts in inflammatory and hyperelastotic lung diseases, the possibility arises that these cells are involved in bronchial pathology, including asthma. To address this issue, we have analyzed by light microscopy, histochemistry and immunohistochemistry the structure of extra- and intra-pulmonary bronchi of patient died of asthma. We have demonstrated hyperplasia of connective tissue cells and fibers in the mucosa, all around the lumen of extra- and intra-pulmonary bronchi. The cells were thin and elongated, labeled by anti-actin and anti-vimentin antibodies and interspersed with many elastic and collagen fibers, therefore they were interpreted as myofibroblasts. These findings may explain the rigidity of the bronchial wall in patients with asthma, which causes the progressively more limited resolution of airway obstruction upon pharmacological treatment and the gross anatomical finding of bronchial stiffness at inspection of the lungs. The possibility should also be considered that myofibroblasts and elastic--not collagen--fibers have contributed to bronchial hyperreactivity at an early stage of the disease.
考虑到肌成纤维细胞在炎症性和高弹性肺部疾病中所起的作用,这些细胞有可能参与包括哮喘在内的支气管病变。为解决这一问题,我们通过光学显微镜、组织化学和免疫组织化学方法分析了死于哮喘患者的肺外和肺内支气管结构。我们发现,在肺外和肺内支气管管腔周围的黏膜中,结缔组织细胞和纤维增生。这些细胞细长,被抗肌动蛋白和抗波形蛋白抗体标记,并散布着许多弹性纤维和胶原纤维,因此被解释为肌成纤维细胞。这些发现可能解释了哮喘患者支气管壁的僵硬,这导致药物治疗后气道阻塞的缓解逐渐受限,以及在肺部检查时支气管僵硬的大体解剖学发现。还应考虑到,在疾病早期,肌成纤维细胞和弹性纤维(而非胶原纤维)可能导致了支气管高反应性。