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Class A scavenger receptor (CD204) attenuates hyperoxia‐induced lung injury by reducing oxidative stress
Author(s) -
Kobayashi H,
Sakashita N,
Okuma T,
Terasaki Y,
Tsujita K,
Suzuki H,
Kodama T,
Nomori H,
Kawasuji M,
Takeya M
Publication year - 2007
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.2150
Subject(s) - hyperoxia , bronchoalveolar lavage , oxidative stress , scavenger receptor , nitrotyrosine , alveolar macrophage , macrophage , lung , nitric oxide synthase , tumor necrosis factor alpha , receptor , nitric oxide , andrology , biology , microbiology and biotechnology , chemistry , immunology , pathology , endocrinology , medicine , in vitro , biochemistry , lipoprotein , cholesterol
To clarify the role of macrophage class A scavenger receptors (SR‐A, CD204) in oxidative lung injury, we examined lung tissue of SR‐A deficient (SR‐A −/− ) and wild‐type (SR‐A +/+ ) mice in response to hyperoxic treatment. Protein levels of bronchoalveolar lavage fluid (BALF) and pulmonary oedema (wet : dry weight ratios) were higher in SR‐A −/− mice than those in SR‐A +/+ mice. Cumulative survival was significantly decreased in SR‐A −/− mice. However, there were no differences in BALF macrophage and neutrophil count between the two groups. Real‐time reverse transcriptase‐polymerase chain reaction (RT‐PCR) revealed that messenger RNA (mRNA) levels of the inducible nitric oxide synthase (iNOS) were increased during hyperoxic injury, and this increase was more prominent in SR‐A −/− mice. Expression levels of iNOS in alveolar macrophages after hyperoxia in vivo and in vitro were higher in SR‐A −/− macrophages compared with SR‐A +/+ macrophages. Immunohistochemistry using anti‐nitrotyrosine antibodies revealed distinctive oxidative stress in the injured lung in both groups, but it was more remarkable in the SR‐A −/− mice. After hyperoxic treatment, pulmonary mRNA levels of tumour necrosis factor‐α(TNF‐α) were elevated more rapidly in SR‐A −/− mice than in SR‐A +/+ mice. Together these results suggest that SR‐A expression attenuates hyperoxia‐induced lung injury by reducing macrophage activation. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.