tetano
Editor, Senior Moderator
Cytokine. 2016 Feb 1;81:23-27. doi: 10.1016/j.cyto.2016.01.016. [Epub ahead of print]
[h=1]Interleukin-35 is upregulated in response to influenza virus infection and secondary bacterial pneumonia.[/h] Chen Y[SUP]1[/SUP], Wang CJ[SUP]1[/SUP], Lin SH[SUP]1[/SUP], Zhang M[SUP]1[/SUP], Li SY[SUP]1[/SUP], Xu F[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Postinfluenza pneumococcal pneumonia is an important cause of global morbidity and mortality. What causes this increased susceptibility is not well elucidated. IL-35 is a newly described cytokine in infectious tolerance. A murine model was established to study postinfluenza pneumococcal pneumonia and evaluate the role of IL-35 in host defense against postinfluenza pneumococcal pneumonia. Pulmonary IL-35 was rapidly up-regulated during murine influenza infection, which was partially mediated by type I IFN-α/β receptor signaling pathway. Secondary pneumococcal infection led to a synergistic IL-35 response in influenza-infected mice. Clinical analysis showed that IL-35 levels were significantly elevated in the patients with influenza infection compared with healthy individuals and influenza infection could induce IL-35 production from human peripheral blood mononuclear cells. These data suggest that IL-35 contributes to the increased susceptibility to secondary pneumococcal pneumonia at least in part by inhibiting the early immune response.
Copyright ? 2016 Elsevier Ltd. All rights reserved.
[h=4]KEYWORDS:[/h] IL-35; Immune response; Infection; Influenza; Pneumonia; Streptococcus pneumoniae
PMID: 26844658 [PubMed - as supplied by publisher]
[h=1]Interleukin-35 is upregulated in response to influenza virus infection and secondary bacterial pneumonia.[/h] Chen Y[SUP]1[/SUP], Wang CJ[SUP]1[/SUP], Lin SH[SUP]1[/SUP], Zhang M[SUP]1[/SUP], Li SY[SUP]1[/SUP], Xu F[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Postinfluenza pneumococcal pneumonia is an important cause of global morbidity and mortality. What causes this increased susceptibility is not well elucidated. IL-35 is a newly described cytokine in infectious tolerance. A murine model was established to study postinfluenza pneumococcal pneumonia and evaluate the role of IL-35 in host defense against postinfluenza pneumococcal pneumonia. Pulmonary IL-35 was rapidly up-regulated during murine influenza infection, which was partially mediated by type I IFN-α/β receptor signaling pathway. Secondary pneumococcal infection led to a synergistic IL-35 response in influenza-infected mice. Clinical analysis showed that IL-35 levels were significantly elevated in the patients with influenza infection compared with healthy individuals and influenza infection could induce IL-35 production from human peripheral blood mononuclear cells. These data suggest that IL-35 contributes to the increased susceptibility to secondary pneumococcal pneumonia at least in part by inhibiting the early immune response.
Copyright ? 2016 Elsevier Ltd. All rights reserved.
[h=4]KEYWORDS:[/h] IL-35; Immune response; Infection; Influenza; Pneumonia; Streptococcus pneumoniae
PMID: 26844658 [PubMed - as supplied by publisher]