title: Characterization of lymphangiogenesis in various stages of idiopathic diffuse alveolar damage.
abstract: In pulmonary fibrosis, an abnormal healing process, is believed to be involved in the damage to lung tissue. This process has not been correlated with lymphangiogenesis, which has garnered current interest in relation to wound healing. The aim of the present study was to clarify the characteristics of lymphangiogenesis in pulmonary fibrosis associated with idiopathic diffuse alveolar damage. Formalin-fixed and paraffin-embedded lung tissues from 13 autopsy cases with idiopathic diffuse alveolar damage were used. Antibodies specific to CD34 and D2-40 were used to detect blood vessels and lymphatics, respectively, and immunohistochemical examinations and morphometry analyses were performed. The standardized density of capillaries was increased significantly in the exudative stage of diffuse alveolar damage, whereas that of the lymphatics remained unchanged. In the proliferative stage, new lymphatics emerged, primarily in the intra-alveolar fibrotic lesions where capillaries were absent. In the fibrotic stage, in which the lung was shrunken, as revealed by the elevated density of pulmonary arteries, the standardized density of capillaries was reduced significantly. The standardized area density of the interstitium was elevated in the proliferative stage and subsequently reduced in the fibrotic stage. Three-dimensional reconstruction of images revealed that some new lymphatics lacked connection to existing lymphatics. During the progression of diffuse alveolar damage, lymphangiogenesis occurs independent of capillary angiogenesis.
authors.affiliation: Department of Pathology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan. yamam@mail.tains.tohoku.ac.jp
authors.forename: Masahiro
authors.initials: M
authors.lastname: Yamashita
authors.forename: Noriyuki
authors.initials: N
authors.lastname: Iwama
authors.forename: Fumiko
authors.initials: F
authors.lastname: Date
authors.forename: Ryoji
authors.initials: R
authors.lastname: Chiba
authors.forename: Masahito
authors.initials: M
authors.lastname: Ebina
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Miki
authors.forename: Kohei
authors.initials: K
authors.lastname: Yamauchi
authors.forename: Takashi
authors.initials: T
authors.lastname: Sawai
authors.forename: Masato
authors.initials: M
authors.lastname: Nose
authors.forename: Shinobu
authors.initials: S
authors.lastname: Sato
authors.forename: Tohru
authors.initials: T
authors.lastname: Takahashi
authors.forename: Masao
authors.initials: M
authors.lastname: Ono
mesh_terms: D000368:Aged; D000911:Antibodies, Monoclonal / Q000378:metabolism; D058846:Antibodies, Monoclonal, Murine-Derived; D018952:Antigens, CD34 / Q000378:metabolism; D005260:Female; D006801:Humans; D054990:Idiopathic Pulmonary Fibrosis / Q000473:pathology*; D007091:Image Processing, Computer-Assisted; D007150:Immunohistochemistry; D042583:Lymphangiogenesis / Q000502:physiology*; D008297:Male; D018919:Neovascularization, Physiologic / Q000502:physiology; D011650:Pulmonary Alveoli / Q000098:blood supply / Q000473:pathology*
chemical_list: D000911:Antibodies, Monoclonal; D058846:Antibodies, Monoclonal, Murine-Derived; D018952:Antigens, CD34; C500987:monoclonal antibody D2-40