Osteopontin Exacerbates Pulmonary Damage in Influenza-Induced Lung Injury

Japanese Journal of Infectious Diseases

Masashi Kohanawa³  Yunan Zhu²  Hongyan Diao²  Yingfeng Wei²  Jianing Chen²  Xuejun Xu¹  Yulong Ding²  Guangying Cui² 

[1] Department of Oral Orthodontics, Affiliated Stomatology Hospital, School of Medicine, Zhejiang University;State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University;Department of Microbiology, School of Medicine, Hokkaido University

关键词: osteopontin;    influenza A virus;    lung injury;    apoptosis;    epithelial sodium channel;   

DOI  :  10.7883/yoken.JJID.2014.467

学科分类：传染病学

来源: National Institute of Infectious Diseases

【 摘 要 】

References(30)Cited-By(2)The level of osteopontin (OPN) increases during bacterial lung infection. However, the OPN level in virus-induced lung injury is unclear, and the relationship between the hyer-production of OPN and lung injury remains to be thoroughly understood. Therefore, we sought to determine whether a relationship exists between OPN and pulmonary damage. Particularly, pulmonary edema and the destruction of pulmonary tissue. In this study, we found that the OPN level was significantly elevated in patients with pulmonary damage, and there was a positive correlation between the OPN serum level and disease severity in influenza lung injury. The epithelial sodium channel (ENaC) is the main mechanism of clearance of pulmonary edema fluid, and matrix metalloproteinase 7 (MMP7) can degrade the extracellular matrix. In lung epithelial cells, OPN markedly decreased the mRNA expression of the α-subunit of ENaC through integrin β3 and CD44 (OPN receptors); however, the expression of MMP7 was promoted by OPN interaction with integrin β1 and CD44. In addition, OPN increased the levels of tumor necrosis factor-α and interleukin-6. These findings suggested that OPN might increase influenza virus-induced lung injury by augmenting lung epithelial cell apoptosis and impairing ENaC and extracellular matrix destruction.

【 授权许可】

Unknown