Interleukin-35 is upregulated in response to influenza virus infection and secondary bacterial pneumonia
Interleukin-35 is upregulated in response to influenza virus infection and secondary bacterial pneumonia
复制标题
Interleukin-35 因流感病毒感染和继发性细菌性肺炎而上调
DOI：
10.1016/j.cyto.2016.01.016
复制
发表时间：
2016-05-01
期刊：
影响因子：
3.8
通讯作者：
Xu, Fang
中科院分区：
文献类型：
--
作者：
Chen, Yi;Wang, Chuan-jiang;Xu, Fang
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-alpha/beta 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. (C) 2016 Elsevier Ltd. All rights reserved.
