Cardiff University | Prifysgol Caerdydd ORCA
Online Research @ Cardiff 
WelshClear Cookie - decide language by browser settings

Viral IL-6 blocks neutrophil infiltration during acute inflammation

Fielding, Ceri Alan, McLoughlin, Rachel Mary, Colmont, Chantal Sophie, Kovaleva, Marina, Harris, Dean Anthony, Rose-John, Stefan, Topley, Nicholas and Jones, Simon Arnett 2005. Viral IL-6 blocks neutrophil infiltration during acute inflammation. The Journal of Immunology 175 (6) , pp. 4024-4029.

Full text not available from this repository.

Abstract

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.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Systems Immunity Research Institute (SIURI)
Publisher: American Association of Immunologists
ISSN: 0022-1767
Last Modified: 10 Oct 2017 12:38
URI: http://orca.cf.ac.uk/id/eprint/231

Citation Data

Cited 20 times in Google Scholar. View in Google Scholar

Cited 22 times in Scopus. View in Scopus. Powered By Scopus® Data

Actions (repository staff only)

Edit Item Edit Item