Viral IL-6 blocks neutrophil infiltration during acute inflammation

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

Research output: Contribution to journalArticlepeer-review

27 Citations (Scopus)


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-1beta-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.
Original languageEnglish
Pages (from-to)4024-9
Number of pages6
JournalThe Journal of Immunology
Issue number6
Publication statusPublished - 15 Sep 2005


  • Acute Disease
  • Animals
  • Bacterial Infections
  • Chemokine CCL2
  • Chemotaxis, Leukocyte
  • Epithelium
  • Herpesvirus 8, Human
  • Immunity, Innate
  • Inflammation
  • Interleukin-1
  • Interleukin-6
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Neutrophils
  • Opportunistic Infections
  • Viral Proteins


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