tetano
Editor, Senior Moderator
[h=1]Expression of inflammation-related genes in the lung of BALB/c mice response to H7N9 influenza A virus with different pathogenicity.[/h] Yu M[SUP]1[/SUP], Wang Q[SUP]1[/SUP], Qi W[SUP]1[/SUP], Zhang K[SUP]1[/SUP], Liu J[SUP]1[/SUP], Tao P[SUP]1[/SUP], Ge S[SUP]1[/SUP], Liao M[SUP]2[/SUP], Ning Z[SUP]3[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] H7N9 influenza A virus (IAV)-infected human cases are increasing and reported over 200 mortalities since its first emergence in 2013. Host inflammatory response contributes to the clearance of influenza virus; meanwhile, the induced "cytokine storm" also leads to pathological lesions. However, what inflammation-related response of the host for H7N9 influenza A virus infection to survival from injures of exuberant cytokine release is still obscure. In this research, expression pattern and histological distribution of inflammation-related genes, RIP3, NLRP3, IL-1β, TNF-α, Slit2 and Robo4 in the lung of BALB/c mice infected with two H7N9 IAV strains with only a PB2 residue 627 difference were investigated, as well as the histopathological injury of the lung. Results showed that significantly higher expression level of NLRP3, RIP3, IL-1β and TNF-α in H7N9-infected groups compared with the control would play a key role in driving lung pathological lesion. While the expression level of Slit2 and Robo4 in H7N9 rV[SUB]K627E[/SUB] group had significantly increased trend than V[SUB]K627[/SUB] which might be the main factor to inhibit the interstitial pneumonia and infiltration. Also, H7N9 induced the histopathological changes in the lung of infected mice, and RIP3, NLRP3, IL-1β, TNF-α, Slit2 and Robo4 showed cell-specific distribution in the lung. The results will provide basic data for further research on the mechanism of inflammatory response and understanding of the role of site 627 in PB2 in H7N9 IAVs infection. In addition, enhancing the resilience of the host vascular system to the inflammatory response by regulation of Slit2-Robo4 signaling pathway might provide a novel strategy for H7N9 IAVs infection.
[h=4]KEYWORDS:[/h] H7N9; IL-1β; Influenza A virus; NLRP3; RIP3; Robo4; Slit2; TNF-α
PMID: 27401907 DOI: 10.1007/s00430-016-0466-x
[PubMed - as supplied by publisher]
[h=3]Author information[/h]
[h=3]Abstract[/h] H7N9 influenza A virus (IAV)-infected human cases are increasing and reported over 200 mortalities since its first emergence in 2013. Host inflammatory response contributes to the clearance of influenza virus; meanwhile, the induced "cytokine storm" also leads to pathological lesions. However, what inflammation-related response of the host for H7N9 influenza A virus infection to survival from injures of exuberant cytokine release is still obscure. In this research, expression pattern and histological distribution of inflammation-related genes, RIP3, NLRP3, IL-1β, TNF-α, Slit2 and Robo4 in the lung of BALB/c mice infected with two H7N9 IAV strains with only a PB2 residue 627 difference were investigated, as well as the histopathological injury of the lung. Results showed that significantly higher expression level of NLRP3, RIP3, IL-1β and TNF-α in H7N9-infected groups compared with the control would play a key role in driving lung pathological lesion. While the expression level of Slit2 and Robo4 in H7N9 rV[SUB]K627E[/SUB] group had significantly increased trend than V[SUB]K627[/SUB] which might be the main factor to inhibit the interstitial pneumonia and infiltration. Also, H7N9 induced the histopathological changes in the lung of infected mice, and RIP3, NLRP3, IL-1β, TNF-α, Slit2 and Robo4 showed cell-specific distribution in the lung. The results will provide basic data for further research on the mechanism of inflammatory response and understanding of the role of site 627 in PB2 in H7N9 IAVs infection. In addition, enhancing the resilience of the host vascular system to the inflammatory response by regulation of Slit2-Robo4 signaling pathway might provide a novel strategy for H7N9 IAVs infection.
[h=4]KEYWORDS:[/h] H7N9; IL-1β; Influenza A virus; NLRP3; RIP3; Robo4; Slit2; TNF-α
PMID: 27401907 DOI: 10.1007/s00430-016-0466-x
[PubMed - as supplied by publisher]