[HTML][HTML] Dengue virus infection activates interleukin-1β to induce tissue injury and vascular leakage

P Pan, Q Zhang, W Wang, G Li, J Wu - Frontiers in Microbiology, 2019 - frontiersin.org
P Pan, Q Zhang, W Wang, G Li, J Wu
Frontiers in Microbiology, 2019frontiersin.org
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 …
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.
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