Open Access

REVIEW

Prokineticin 1 induces CCL4, CXCL1 and CXCL8 in human monocytes but not in macrophages and dendritic cells

Justin Monnier¹, Véronique Quillien², Claire Piquet-Pellorce³, Claudine Leberre⁴, Laurence Preisser⁵, Hugues Gascan⁵, Michel Samson¹

1 INSERM U620; Université de Rennes 1, IFR140, Rennes
2 UMR 6061 CNRS, Centre Eugene Marquis, Rennes
3 INSERM U522, Rennes
4 EFS, Rennes
5 INSERM U564, Angers, France

* Corresponding Author: M. Samson,

European Cytokine Network 2008, 19(4), 166-175. https://doi.org/10.1684/ecn.2008.0138

Accepted 27 October 2008;

Abstract

Prokineticin 1 and 2 (PROK1 and PROK2) are two small proteins largely expressed in inflamma-tory tissues and involved in monocyte activation and differentiation. The focus of this study was to evaluate whether PROK1 was able to induce chemokine secretion in human monocytes, in monocyte-derived macro-phages and in monocyte-derived dendritic cells, an aspect not addressed thus far. Here, we show for the first time, using flow cytometry, that PROK receptors 1 and 2 are present on the surface of human monocytes. Sub-sequently, monocytes were selected to investigate the chemokine response after stimulation by PROK1. Our results show that only three chemokines (CCL4, CXCL1 and CXCL8) were significantly induced at both the transcript and protein level, and that PROK1 induces most potently CXCL8, in a dose-dependent manner. From a mechanistic point of view, by blocking independently Gαi protein or intracellular calcium, monocytes lose the ability to secrete CXCL8 in response to PROK1. Finally, we observed that CCL4, CXCL1 and CXCL8 secretion, following PROK1 induction, is only observed in monocytes and not in monocyte-derived macrophages and dendritic cells. Our results demonstrate that, in vitro, the differentiation status of monocytes influences che-mokine production after stimulation by PROK1, and that this chemokine production is geared toward a pro-inflammatory response. This could represent a novel amplification loop of leukocyte recruitment, extravasation and tissue invasion.

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Keywords

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