In this study, we demonstrated that p38 MAPK-mediated matrix metalloproteinase-13 expression by influenza A virus infection led to destabilization of vulnerable atherosclerotic plaques in artery.(191 words).
In this study, we demonstrated that p38 MAPK-mediated matrix metalloproteinase-13 expression by influenza A virus infection led to destabilization of vulnerable atherosclerotic plaques in artery.(191 words).
In this study, we demonstrated that p38 MAPK-mediated matrix metalloproteinase-13 expression by influenza A virus infection led to destabilization of vulnerable atherosclerotic plaques in artery.(191 words).
In this study, we demonstrated that p38 MAPK-mediated matrix metalloproteinase-13 expression by influenza A virus infection led to destabilization of vulnerable atherosclerotic plaques in artery.(191 words).
In this study, we demonstrated that p38 MAPK-mediated matrix metalloproteinase-13 expression by influenza A virus infection led to destabilization of vulnerable atherosclerotic plaques in artery.(191 words).
In this study, we demonstrated that p38 MAPK-mediated matrix metalloproteinase-13 expression by influenza A virus infection led to destabilization of vulnerable atherosclerotic plaques in artery.(191 words).
In this study, we demonstrated that p38 MAPK-mediated matrix metalloproteinase-13 expression by influenza A virus infection led to destabilization of vulnerable atherosclerotic plaques in artery.(191 words).
In this study, we demonstrated that p38 MAPK-mediated matrix metalloproteinase-13 expression by influenza A virus infection led to destabilization of vulnerable atherosclerotic plaques in artery.(191 words).
In this study, we demonstrated that p38 MAPK-mediated matrix metalloproteinase-13 expression by influenza A virus infection led to destabilization of vulnerable atherosclerotic plaques in artery.(191 words).
We demonstrate here that while IL-5 is required for optimal recovery from influenza A virus infection in BALB/c and C57BL/6 mice, the protective effect of IL-5 is independent of eosinophils, suggesting an alternative cellular target.
In contrast, inhibition of the PI3K/AKT pathway or overexpression of Beclin1 reduced the number of S. pneumoniae population, the activity of MPO, and the expression of TNF-α, IL-6, and IFN-γ in BALF of mice reinfected with S. pneumoniae after influenza A virus infection.
Collectively, our study demonstrates that inhibition of the PI3K/AKT signaling pathway or overexpressed Beclin1 alleviates reinfection of S. pneumoniae after influenza A virus infection in SCAP.
Collectively, our study demonstrates that inhibition of the PI3K/AKT signaling pathway or overexpressed Beclin1 alleviates reinfection of S. pneumoniae after influenza A virus infection in SCAP.
In contrast, inhibition of the PI3K/AKT pathway or overexpression of Beclin1 reduced the number of S. pneumoniae population, the activity of MPO, and the expression of TNF-α, IL-6, and IFN-γ in BALF of mice reinfected with S. pneumoniae after influenza A virus infection.
In contrast, inhibition of the PI3K/AKT pathway or overexpression of Beclin1 reduced the number of S. pneumoniae population, the activity of MPO, and the expression of TNF-α, IL-6, and IFN-γ in BALF of mice reinfected with S. pneumoniae after influenza A virus infection.
In contrast, inhibition of the PI3K/AKT pathway or overexpression of Beclin1 reduced the number of S. pneumoniae population, the activity of MPO, and the expression of TNF-α, IL-6, and IFN-γ in BALF of mice reinfected with S. pneumoniae after influenza A virus infection.
Collectively, our study demonstrates that inhibition of the PI3K/AKT signaling pathway or overexpressed Beclin1 alleviates reinfection of S. pneumoniae after influenza A virus infection in SCAP.