Osteopontin Exacerbates Pulmonary Damage in Influenza-Induced Lung Injury

Zhu, Yunan; Wei, Yu; Chen, Jianing; Cui, Guangying; Ding, Yuhao; Kohanawa, Masashi; Xu, Xuejun; Diao, Hongyan

doi:10.7883/yoken.jjid.2014.467

Cited by 13 publications

(8 citation statements)

References 28 publications

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“…OPN up-regulation in serum and tissue samples from chronic rhinosinusitis and allergic patients also correlated with severity of disease [ 55 , 60 , 61 ]. In agreement with these studies, a recent paper found a positive correlation between increased levels of OPN in human serum and disease severity in influenza patients [ 62 ]. Our in vitro finding suggests that IFN-β reduces the viral infection resulting in decreased IL-1 β and OPN expression and is consistent with previous reports where RSV-A2 infection resulted in significantly higher expression of IFN-α than RSV-L19F in human epithelial cells and BALB/c mice [ 45 , 63 ].…”

Section: Discussionsupporting

confidence: 79%

Osteopontin plays a pivotal role in increasing severity of respiratory syncytial virus infection

et al. 2018

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The molecular mechanisms underlying susceptibility to severe respiratory syncytial virus (RSV) infection remain poorly understood. Herein, we report on the role of osteopontin (OPN) in regulation of RSV infection in human epithelial cells and how interleukin-1 beta (IL-1β), a cytokine secreted soon after RSV infection, when persistently expressed can induce OPN expression leading to increased viral infection. We first compared OPN expression in two human epithelial cell lines: HEK-293 and HEp-2. In contrast to HEp-2, HEK-293 expresses low levels of pro-caspase-1 resulting in decreased IL-1β expression in response to RSV infection. We found a correlation between low IL-1β levels and a delay in induction of OPN expression in RSV-infected HEK-293 cells compared to HEp-2. This phenomenon could partially explain the high susceptibility of HEp-2 cells to RSV infection versus the moderate susceptibility of HEK-293 cells. Also, HEK-293 cells expressing low levels of pro-caspase-1 exhibit decreased IL-1β expression and delayed OPN expression in response to RSV infection. HEK-293 cells incubated with human rIL-1β showed a dose-dependent increase in OPN expression upon RSV infection. Also, incubation with rOPN increased RSV viral load. Moreover, HEp-2 cells or mice infected with a mucogenic RSV strain RSV-L19F showed elevated levels of OPN in contrast to mice infected with the laboratory RSV strain rA2. This correlated with elevated levels of OPN following infection with RSV-L19F compared to rA2. Together, these results demonstrate that increased OPN expression is regulated in part by IL-1β, and the interplay between IL-1β and OPN signaling may play a pivotal role in the spread of RSV infection.

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Section: Discussionsupporting

confidence: 79%

Osteopontin plays a pivotal role in increasing severity of respiratory syncytial virus infection

et al. 2018

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“… 30 And our previous study inferred MMP7 could play an important role in influenza infection. 31 At 1 month postinfection, we found higher plasma levels of MMP2, MMP3, and MMP9 in survivors of severe H7N9 infection. It is possible that ongoing tissue remodeling adds to the feeble recovery seen after severe H7N9 infection.…”

Section: Discussionmentioning

confidence: 58%

Severe Infection With Avian Influenza A Virus is Associated With Delayed Immune Recovery in Survivors

Chen

Cui

Lu³

et al. 2016

Medicine

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“…There are only a few studies of the relationship between OPN and SHP. OPN can induce a significant increase in the level of tumour necrosis factor α (TNFα) in mice 42 . TNFα can also activate the c-Jun N-terminal kinase (JNK) pathway 43 .…”

Section: Discussionmentioning

confidence: 99%

Osteopontin Deficiency Alters Biliary Homeostasis and Protects against Gallstone Formation

Lin

Lü

Shao

et al. 2016

Sci Rep

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The precipitation of excess biliary cholesterol as solid crystals is a prerequisite for cholesterol gallstone formation, which occurs due to disturbed biliary homeostasis. Biliary homeostasis is regulated by an elaborate network of genes in hepatocytes. If unmanaged, the cholesterol crystals will aggregate, fuse and form gallstones. We have previously observed that the levels of osteopontin (OPN) in bile and gallbladder were reduced in gallstone patients. However, the role and mechanism for hepatic OPN in cholesterol gallstone formation is undetermined. In this study, we found that the expression of hepatic OPN was increased in gallstone patients compared with gallstone-free counterparts. Then, we observed that OPN-deficient mice were less vulnerable to cholesterol gallstone formation than wild type mice. Further mechanistic studies revealed that this protective effect was associated with alterations of bile composition and was caused by the increased hepatic CYP7A1 expression and the reduced expression of hepatic SHP, ATP8B1, SR-B1 and SREBP-2. Finally, the correlations between the expression of hepatic OPN and the expression of these hepatic genes were validated in gallstone patients. Taken together, our findings reveal that hepatic OPN contributes to cholesterol gallstone formation by regulating biliary metabolism and might be developed as a therapeutic target for gallstone treatments.

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Osteopontin Exacerbates Pulmonary Damage in Influenza-Induced Lung Injury

Cited by 13 publications

References 28 publications

Osteopontin plays a pivotal role in increasing severity of respiratory syncytial virus infection

Osteopontin plays a pivotal role in increasing severity of respiratory syncytial virus infection

Severe Infection With Avian Influenza A Virus is Associated With Delayed Immune Recovery in Survivors

Osteopontin Deficiency Alters Biliary Homeostasis and Protects against Gallstone Formation

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