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International Immunology Advance Access originally published online on January 10, 2008
International Immunology 2008 20(3):327-336; doi:10.1093/intimm/dxm145
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© The Japanese Society for Immunology. 2008. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Prolactin-induced production of cytokines in macrophages in vitro involves JAK/STAT and JNK MAPK pathways

Anurag Tripathi and Ajit Sodhi

School of Biotechnology, Faculty of Science, Banaras Hindu University, Varanasi 221005, India

Correspondence to: A. Sodhi; E-mail: ajit.sodhi{at}lycos.com

Macrophages play a crucial role in host immunosurveillance against pathogens and malignancies. The enhanced productions of pro-inflammatory cytokines are central to the regulatory role of macrophages and induction of robust immune response. The excessive inflammatory response of macrophages can result into pathological conditions in host. We have previously reported that prolactin (PRL) induces the production of nitric oxide (NO) and tumor necrosis factor (TNF)-{alpha} in murine peritoneal macrophages. It was suggested that protein tyrosine kinases (PTKs), mitogen-activated protein kinases (MAPKs) and Ca++ signaling were involved in the NO production by macrophages on PRL treatment. In this manuscript, we investigated the role of PTKs [Janus kinase (JAK) 2 and phosphoinositide 3-kinase (PI3K)] and c-Jun N-terminal kinase (JNK) MAPK in PRL-induced activation of murine peritoneal macrophages. It is reported that PRL-induced activation of macrophages in vitro is dependent on JAK/signal transducers and activators of transcription (STAT) and JNK MAPK-signaling pathways. It is observed that pre-treatment of macrophages with JNK inhibitor, SP600125; tyrosine kinase inhibitor, genistein; PI3K inhibitor, Wortmannin and JAK2 inhibitor, AG490 inhibited the phosphorylation of JNK MAPK. Further, pre-treatment of macrophages with SP600125 inhibited the PRL-induced production of IFN-{gamma} and TNF-{alpha}. AG490, inhibitor of JAK2, down-regulated transcription factors c-jun and STAT1 and inhibited the PRL-induced IFN-{gamma}, TNF-{alpha}, IL-1β and IL-12p40 production in macrophages.

Keywords: macrophage activation, signal transduction

Transmitting editor: A. Falus

Received 15 September 2007, accepted 7 December 2007.


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