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Viral IL-6 Blocks Neutrophil Infiltration during Acute Inflammation¹

Ceri A. Fielding^*, Rachel M. McLoughlin^*,, Chantal S. Colmont, Marina Kovaleva, Dean A. Harris, Stefan Rose-John, Nicholas Topley and Simon A. Jones^2,*

^* Department of Medical Biochemistry and Immunology and Department of Nephrology, School of Medicine, Cardiff University, Wales, United Kingdom; and Department of Biochemistry, Christian-Albrechts-Universtitat zu Kiel, Kiel, Germany

Pathologies arising as a consequence of human herpesvirus-8 (HHV8) infections are closely associated with the autocrine activity of a HHV8 encoded IL-6 (vIL-6), which promotes proliferation of infected cells and their resistance to apoptosis. In this present report, studies show that vIL-6 may also be important in influencing the host’s immunological response to secondary infections. Using peritoneal inflammation as a model of acute bacterial infection, vIL-6 was found to specifically block neutrophil recruitment in vivo through regulation of inflammatory chemokine expression. This response was substantiated in vitro where activation of STAT3 in human peritoneal mesothelial cells by vIL-6 was associated with enhanced CCL2 release. Although vIL-6 did not effect CXCL8 production, IL-1-induced secretion of this neutrophil-activating chemokine was significantly suppressed by vIL-6. These data suggest that vIL-6 has the capacity to suppress innate immune responses and thereby influence the outcome of opportunistic infections in HHV8-associated disease.

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