Dengue Virus Infection Activates Interleukin-1β to Induce Tissue Injury and Vascular Leakage
oleh: Pan Pan, Qi Zhang, Weiyong Liu, Wenbiao Wang, Zhenyang Yu, Zizhao Lao, Wei Zhang, Miaomiao Shen, Pin Wan, Feng Xiao, Muhammad Adnan Shereen, Wen Zhang, Qiuping Tan, Yuntao Liu, Xiaohong Liu, Kailang Wu, Yingle Liu, Yingle Liu, Geng Li, Jianguo Wu, Jianguo Wu
| Format: | Article |
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| Diterbitkan: | Frontiers Media S.A. 2019-11-01 |
Deskripsi
Dengue virus (DENV) infection causes several diseases ranging from dengue fever to life-threatening dengue hemorrhagic fever and dengue shock syndrome characterized by endothelial dysfunction, vascular leakage, and shock. Here, we identify a potential mechanism by which DENV induces tissue injury and vascular leakage by promoting the activation of interleukin (IL)-1β. DENV facilitates IL-1β secretion in infected patients, mice, human peripheral blood mononuclear cells (PBMCs), mouse bone marrow-derived macrophages (BMDMs), and monocyte-differentiated macrophages (THP-1) via activating the NLRP3 inflammasome. The accumulated data suggest that IL-1β probably induces vascular leakage and tissue injury in interferon-alpha/beta receptor 1 deficient C57BL/6 mice (IFNAR–/– C57BL/6), whereas IL-1 receptor antagonist (IL-1RA) alleviates these effects of IL-1β. Finally, administration of recombinant IL-1β protein results in vascular leakage and tissue injury in C57BL/6 mice. Together, the accumulated results demonstrate that IL-1β contributes to DENV-associated pathology and suggest that IL-1RA acts as a potential agent for the treatment of DENV-associated diseases.