The Role of Catalase in Pulmonary Fibrosis

Nao Odajima, Tomoko Betsuyaku, Katsura Nagai, Chinatsu Moriyama, Da Hong Wang, Tomoko Takigawa, Keiki Ogino, Masaharu Nishimura

Research output: Contribution to journalArticlepeer-review

43 Citations (Scopus)


Background: Catalase is preferentially expressed in bronchiolar and alveolar epithelial cells, and acts as an endogenous antioxidant enzyme in normal lungs. We thus postulated epithelial damage would be associated with a functional deficiency of catalase during the development of lung fibrosis.Methods: The present study evaluates the expression of catalase mRNA and protein in human interstitial pneumonias and in mouse bleomycin-induced lung injury. We examined the degree of bleomycin-induced inflammation and fibrosis in the mice with lowered catalase activity.Results: In humans, catalase was decreased at the levels of activity, protein content and mRNA expression in fibrotic lungs (n = 12) compared to control lungs (n = 10). Immunohistochemistry revealed a decrease in catalase in bronchiolar epithelium and abnormal re-epithelialization in fibrotic areas. In C57BL/6J mice, catalase activity was suppressed along with downregulation of catalase mRNA in whole lung homogenates after bleomycin administration. In acatalasemic mice, neutrophilic inflammation was prolonged until 14 days, and there was a higher degree of lung fibrosis in association with a higher level of transforming growth factor-β expression and total collagen content following bleomycin treatment compared to wild-type mice.Conclusions: Taken together, these findings demonstrate diminished catalase expression and activity in human pulmonary fibrosis and suggest the protective role of catalase against bleomycin-induced inflammation and subsequent fibrosis.

Original languageEnglish
Article number183
JournalRespiratory Research
Publication statusPublished - 2010 Dec 29
Externally publishedYes

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine


Dive into the research topics of 'The Role of Catalase in Pulmonary Fibrosis'. Together they form a unique fingerprint.

Cite this