tetano
Editor, Senior Moderator
Front Microbiol. 2017 Apr 4;8:587. doi: 10.3389/fmicb.2017.00587. eCollection 2017.
[h=1]C-C Motif Chemokine Ligand 2 (CCL2) Mediates Acute Lung Injury Induced by Lethal Influenza H7N9 Virus.[/h] Lai C[SUP]1[/SUP], Wang K[SUP]1[/SUP], Zhao Z[SUP]1[/SUP], Zhang L[SUP]1[/SUP], Gu H[SUP]1[/SUP], Yang P[SUP]1,[/SUP][SUP]2[/SUP], Wang X[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] An avian-origin influenza A (H7N9) virus was a cause for concern in China in the spring of 2013. Most H7N9 infections resulted in acute respiratory distress syndrome (ARDS), which is a severe form of acute lung injury (ALI) that contributes to morbidity and mortality. In this study, we induced viral ALI by infecting wild-type and CCL2-deficient mice with influenza H7N9 virus. The results suggested a close association between C-C motif chemokine ligand 2 (CCL2) expressions and ALI induced by a lethal H7N9 virus strain (A/Hebei/01/2013). Elevated CCL2 levels were also detected in confirmed human cases of H7N9 and the bronchoalveolar lavage fluid (BALF) of H7N9-infected mice. Moreover, CCL2 was overexpressed in the lung tissue of infected mice. More importantly, CCL2 deficiency ameliorated H7N9-induced ALI in mice as determined by weight loss, survival rate, the wet:dry ratio of the lung, and pathology. Taken together, our findings demonstrate that CCL2 is essential for H7N9 virus infection and thus that it is a potential therapeutic target for influenza.
[h=4]KEYWORDS:[/h] CCL2; acute lung injury (ALI); experimental mouse model; influenza H7N9 Hb01 virus; lethal influenza H7N9 virus
PMID: 28421067 PMCID: PMC5379033 DOI: 10.3389/fmicb.2017.00587
Free PMC Article
[h=1]C-C Motif Chemokine Ligand 2 (CCL2) Mediates Acute Lung Injury Induced by Lethal Influenza H7N9 Virus.[/h] Lai C[SUP]1[/SUP], Wang K[SUP]1[/SUP], Zhao Z[SUP]1[/SUP], Zhang L[SUP]1[/SUP], Gu H[SUP]1[/SUP], Yang P[SUP]1,[/SUP][SUP]2[/SUP], Wang X[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] An avian-origin influenza A (H7N9) virus was a cause for concern in China in the spring of 2013. Most H7N9 infections resulted in acute respiratory distress syndrome (ARDS), which is a severe form of acute lung injury (ALI) that contributes to morbidity and mortality. In this study, we induced viral ALI by infecting wild-type and CCL2-deficient mice with influenza H7N9 virus. The results suggested a close association between C-C motif chemokine ligand 2 (CCL2) expressions and ALI induced by a lethal H7N9 virus strain (A/Hebei/01/2013). Elevated CCL2 levels were also detected in confirmed human cases of H7N9 and the bronchoalveolar lavage fluid (BALF) of H7N9-infected mice. Moreover, CCL2 was overexpressed in the lung tissue of infected mice. More importantly, CCL2 deficiency ameliorated H7N9-induced ALI in mice as determined by weight loss, survival rate, the wet:dry ratio of the lung, and pathology. Taken together, our findings demonstrate that CCL2 is essential for H7N9 virus infection and thus that it is a potential therapeutic target for influenza.
[h=4]KEYWORDS:[/h] CCL2; acute lung injury (ALI); experimental mouse model; influenza H7N9 Hb01 virus; lethal influenza H7N9 virus
PMID: 28421067 PMCID: PMC5379033 DOI: 10.3389/fmicb.2017.00587
Free PMC Article