title: Enhanced mast cell chymase expression in human idiopathic interstitial pneumonia.
abstract: Previous studies have shown that mast cell chymase induces and promotes fibrogenesis in injured tissues. We studied the roles of mast cell chymase in the fibritic processes of human idiopathic interstitial pneumonias. Frozen tissue sections from human lungs with usual interstitial pneumonia (n=7), nonspecific interstitial pneumonia (n=4) and normal lungs (n=10) were studied immunohistochemically. Monoclonal antibodies against mast cell chymase, tryptase, interleukin-4, and smooth muscle actin were used. Stained cells or areas were quantified by computer-aided morphometry. The numbers of both tryptase-positive mast cells and chymase-positive mast cells were significantly greater in lung tissues with idiopathic interstitial pneumonia than in normal lung tissues. The increase in the number of chymase-positive mast cells in the diseased lung tissues was closely related to an increase in interleukin-4-positive cells, and also to an accumulation of smooth muscle cells and myofibroblasts. Because smooth muscle cell and myofibroblast proliferation is a principal pathological change in idiopathic interstitial pneumonias, these observations suggest that mast cell chymase, possibly induced by interleukin-4-dependent phenotypic modulation, may be an important mediator in the inflammatory and fibrotic processes of idiopathic interstitial pneumonia in humans.
authors.affiliation: Department of Respiratory Medicine, Osaka City University Graduate School of Medicine, Osaka 545-8585, Japan. kazutoh@msic.med.osaka-cu.ac.jp
authors.forename: Kazuto
authors.initials: K
authors.lastname: Hirata
authors.forename: Yoshimi
authors.initials: Y
authors.lastname: Sugama
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Ikura
authors.forename: Masahiko
authors.initials: M
authors.lastname: Ohsawa
authors.forename: Yoshikazu
authors.initials: Y
authors.lastname: Inoue
authors.forename: Satoru
authors.initials: S
authors.lastname: Yamamoto
authors.forename: Masanori
authors.initials: M
authors.lastname: Kitaichi
authors.forename: Makiko
authors.initials: M
authors.lastname: Ueda
mesh_terms: D000199:Actins / Q000032:analysis; D000368:Aged; D049109:Cell Proliferation; D053818:Chymases / Q000032:analysis / Q000502:physiology*; D005260:Female; D005347:Fibroblasts / Q000473:pathology; D005355:Fibrosis; D006801:Humans; D007150:Immunohistochemistry; D015847:Interleukin-4 / Q000032:analysis / Q000378:metabolism; D017563:Lung Diseases, Interstitial / Q000201:enzymology / Q000209:etiology* / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D032389:Myocytes, Smooth Muscle / Q000737:chemistry / Q000473:pathology
chemical_list: D000199:Actins; D015847:Interleukin-4; C509226:CMA1 protein, human; D053818:Chymases