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The Journal of Immunology, 2002, 169: 5244-5251.
Copyright © 2002 by The American Association of Immunologists

Secretion of Oncostatin M by Infiltrating Neutrophils: Regulation of IL-6 and Chemokine Expression in Human Mesothelial Cells1

Suzanne M. Hurst2,*, Rachel M. McLoughlin*,{dagger}, James Monslow*, Sara Owens{dagger}, Llinos Morgan{dagger}, Gerald M. Fuller{ddagger}, Nicholas Topley{dagger} and Simon A. Jones*

* Cardiff School of Biosciences, Cardiff University, {dagger} Institute of Nephrology, University of Wales College of Medicine, Cardiff, United Kingdom; and {ddagger} Department of Cell Biology, University of Alabama, Birmingham, AL 35294

Recently, we identified that regulation of leukocyte recruitment by IL-6 requires shedding of the IL-6R from infiltrating neutrophils. In this study, experiments have examined whether other IL-6-related cytokines possess similar properties. Levels of oncostatin M (OSM) and leukemia inhibitory factor were analyzed in patients with overt bacterial peritonitis during the first 5 days of infection. Although no change in leukemia inhibitory factor was observed throughout the duration of infection, OSM was significantly elevated on day 1 and rapidly returned to baseline by days 2–3. The source of OSM was identified as the infiltrating neutrophils, and OSM levels correlated both with leukocyte numbers and i.p. soluble IL-6R (sIL-6R) levels. FACS analysis revealed that OSM receptor {beta} expression was restricted to human peritoneal mesothelial cells. Stimulation of human peritoneal mesothelial cells with OSM induced phosphorylation of gp130 and OSM receptor {beta}, which was accompanied by activation of STAT3 and secretion of CC chemokine ligand 2/monocyte chemoattractant protein-1 and IL-6. Although OSM itself did not modulate CXC chemokine ligand 8/IL-8 release, it effectively suppressed IL-1{beta}-mediated expression of this neutrophil-activating CXC chemokine. Moreover, OSM synergistically blocked IL-1{beta}-induced CXC chemokine ligand 8 secretion in combination with the IL-6/sIL-6R complex. Thus suggesting that OSM and sIL-6R release from infiltrating neutrophils may contribute to the temporal switch between neutrophil influx and mononuclear cell recruitment seen during acute inflammation.




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