tetano
Editor, Senior Moderator
Jpn J Infect Dis. 2015 Apr 10. [Epub ahead of print]
[h=1]Osteopontin exacerbates pulmonary damage in influenzal lung injury.[/h] Zhu Y[SUP]1[/SUP], Wei Y, Chen J, Cui G, Ding Y, Kohanawa M, Xu X, Diao H.
[h=3]Author information[/h]
[h=3]Abstract[/h] Osteopontin (OPN) is increased in bacterial lung infection. However, the level of OPN in virus-induced lung injury is not clear and the relationship between the hyerproduction of osteopontin and lung injury remains to be thoroughly understood. Therefore, we sought to determine whether there is any relationship between OPN and pulmonary damage, particularly, pulmonary edema and destruction of pulmonary tissue. In this study, we found OPN level was significantly elevated in patients with pulmonary damage and there was a positive correlation between serum level of OPN and disease severity in influenza lung injury. The epithelial sodium channel (ENaC) is the main mechanism of clearance of pulmonary edema fluid and matrix metalloproteinase7 (MMP7) is able to degrade extracellular matrix. In lung epithelial cells, OPN markedly decreased the expression of α-subunit of ENaC mRNA through the integrin β3 and CD44 (the osteopontin receptors), however, the expression of MMP7 was promoted by OPN interacted with integrin β1 and CD44. In addition, the levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were increased by OPN. These findings suggested that OPN may increase influenza virus-induced lung injury through augment lung epithelial cells apoptosis and impaired the epithelial sodium channel, as well as extracellular matrix destruction.
PMID: 25866117 [PubMed - as supplied by publisher]
[h=1]Osteopontin exacerbates pulmonary damage in influenzal lung injury.[/h] Zhu Y[SUP]1[/SUP], Wei Y, Chen J, Cui G, Ding Y, Kohanawa M, Xu X, Diao H.
[h=3]Author information[/h]
[h=3]Abstract[/h] Osteopontin (OPN) is increased in bacterial lung infection. However, the level of OPN in virus-induced lung injury is not clear and the relationship between the hyerproduction of osteopontin and lung injury remains to be thoroughly understood. Therefore, we sought to determine whether there is any relationship between OPN and pulmonary damage, particularly, pulmonary edema and destruction of pulmonary tissue. In this study, we found OPN level was significantly elevated in patients with pulmonary damage and there was a positive correlation between serum level of OPN and disease severity in influenza lung injury. The epithelial sodium channel (ENaC) is the main mechanism of clearance of pulmonary edema fluid and matrix metalloproteinase7 (MMP7) is able to degrade extracellular matrix. In lung epithelial cells, OPN markedly decreased the expression of α-subunit of ENaC mRNA through the integrin β3 and CD44 (the osteopontin receptors), however, the expression of MMP7 was promoted by OPN interacted with integrin β1 and CD44. In addition, the levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were increased by OPN. These findings suggested that OPN may increase influenza virus-induced lung injury through augment lung epithelial cells apoptosis and impaired the epithelial sodium channel, as well as extracellular matrix destruction.
PMID: 25866117 [PubMed - as supplied by publisher]