Production of interleukin-1 (IL-1) and IL-1 inhibitor by human monocytes exposed to dengue virus.
Dengue hemorrhagic fever-dengue shock syndrome, the most severe manifestation of an acute dengue virus (DV) infection, is endemic in Southeast Asia. Antibody-dependent enhancement of DV growth in mononuclear phagocytes is thought to be the mechanism whereby preexisting dengue antibodies confer excess risk for this outcome. Interleukin-1 (IL-1) may play an important role in the pathogenetic mechanisms that cause dengue fever and shock. It was shown that both IL-1 and tumor necrosis factor-alpha are secreted from monocytes within 4 h after DV infection. However, there was no increase in IL-1 secretion by virus-stimulated monocytes from dengue fever patients compared with healthy controls. Significant amounts of IL-1 were secreted by DV-infected monocytes in the presence of aggregated immunoglobulin or immune complexes. In addition, a new 600-kDa IL-1 inhibitor from the supernatants of DV-infected monocytes was identified. This inhibitor may cause immunosuppression and influence the process of DV infection.
Chang
D M
DM
Division of Rheumatology/Immunology/Allergy, Tri-Service General Hospital, Taipei, Taiwan, R.O.C.
Shaio
M F
MF
D001210:Asia, Southeastern / Q000453:epidemiology; D002448:Cell Adhesion; D003715:Dengue / Q000453:epidemiology; D003716:Dengue Virus / Q000276:immunology*; D006801:Humans; D007108:Immune Tolerance; D066298:In Vitro Techniques; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1 / Q000096:biosynthesis* / Q000097:blood; D009000:Monocytes / Q000276:immunology / Q000821:virology*; D012307:Risk Factors; D012795:Sialoglycoproteins / Q000096:biosynthesis* / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha