Abstract
Pulmonary fibrosis is a terminal productive phase. Pulmonary fibrosis occurs in inflammation scars and in emphysema of the lung. It is a proliferation of collagen fiber as a result of increase of fibroblasts. Myofibroblasts and collagen type III constitute the proliferative linkage. Collagen type III turns into collagen type I in the phase in which fibroblast turns into myofibroblast. Collagen type III is prominent in immature connective tissue. Collagen type I is prominent in mature conncetive tissue. We studied changes of the bronchus by light microscopy, electron microscopy and immunohistochemistry, especially the fibrosis of mucous membrane of the bronchus, the basement membrane, the peribronchial area and smooth muscle of the bronchus, after inhalation of antigen. Immunohistochemistry was used with anti-collagen type III monoclonal antibody, anti-laminin polyclonal antibody, anti-fibronectin polyclonal antibody and anti-smooth muscle monoclonal antibody. In the early phase of fibrosis of the bronchial wall, anti-collagen type III monoclonal antibody increased sensitivity in the subepithelial lesion of the bronchus and in the perimuscular connective tissue of the bronchus. Electron microscopy proved that fibroblasts and myofibroblasts were in the same lesions of the bronchus. Fibrosis of the bronchial lesion is gradually accelarated by an attack of asthma, except inflammation.
