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International Immunology Advance Access originally published online on February 27, 2008
International Immunology 2008 20(4):535-541; doi:10.1093/intimm/dxn015
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© The Japanese Society for Immunology. 2008. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Circulating neutrophils of septic patients constitutively express IL-10R1 and are promptly responsive to IL-10

Nicola Tamassia1, Federica Calzetti1, Nicola Menestrina2, Marzia Rossato1, Flavia Bazzoni1, Leonardo Gottin2 and Marco A. Cassatella1

1 Department of Pathology, Division of General Pathology and
2 Department of Anaesthetic Science and Specialized Surgery, University of Verona, Verona, Italy

Correspondence to: M. A. Cassatella; E-mail: marco.cassatella{at}univr.it

Previous studies have demonstrated that neutrophils isolated from the blood of healthy donors do not respond to IL-10 in terms of either activation of signal transducer and activator of transcription-3 (STAT3) tyrosine phosphorylation or induction of suppressor of cytokine signalling (SOCS)-3 protein, unlike autologous mononuclear cells. This was explained by the fact that circulating neutrophils of healthy donors express only IL-10R2, but not IL-10R1, the latter IL-10R chain being essential for mediating IL-10 responsiveness. In this study, we report that peripheral blood neutrophils of septic patients constitutively display, besides IL-10R2, also abundant levels of surface IL-10R1. Consequently, septic neutrophils are promptly responsive to IL-10 in vitro, as revealed by a direct IL-10-mediated induction of STAT3 tyrosine phosphorylation and SOCS-3 gene transcription, mRNA and protein expression. Consistent with the presence of a fully functional IL-10R, modulation of LPS-induced CXCL8, CCL4, tumour necrosis factor-{alpha} and IL-1ra gene expression was also rapidly induced by IL-10 in septic, but not normal, neutrophils. Collectively, these data uncover that neutrophils of septic patients are predisposed to be promptly responsive to IL-10, presumably to help limiting their pro-inflammatory state. They also fully validate our previous observations, herein in the context of a human disease, that responsiveness of human neutrophils to IL-10 is strictly dependent upon the modulation of IL-10R1 expression.

Keywords: IL-1ra, IL-10R1, lipopolysaccharide, neutrophils, SOCS-3, TNF-{alpha}

Transmitting editor: G. Trinchieri

Received 14 December 2007, accepted 23 January 2008.


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