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1 Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, University of California, Davis, CA, USA
2 Department of Internal Medicine, Division of Nephrology, University of California, Davis, CA, USA
3 Department of Internal Medicine, Division of Rheumatology/Allergy, University of California, Davis, CA, USA
4 Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine, University of California, Davis, CA, USA; Department of Human Physiology, University of California, Davis, CA, USA
* To whom correspondence should be addressed. E-mail: amcorbacho{at}ucdavis.edu.
Acute inflammation can elicit a defense reaction, known as the acute phase
response (APR) that is crucial for re-establishing homeostasis in the host. The role for
prolactin (PRL) as an immunomodulatory factor maintaining homeostasis under
conditions of stress has been proposed, however its function during the APR remains
unclear. Previously, it was shown that pro-inflammatory cytokines characteristic of the
APR (TNF
, IL-1
and IFN
) induced the expression of the PRL receptor (PRLR) by
pulmonary fibroblasts in vitro. Here, we investigated the in vivo expression of PRLR
during lipopolysaccharide (LPS)-induced APR in various tissues of the mouse. We show
that PRLR mRNA and protein levels were down-regulated in hepatic tissues after i.p.
LPS-injection. Down-regulation of PRLR in the liver was confirmed by
immunohistochemistry. A suppressive effect on mRNA expression was also observed in
prostate, seminal vesicle, kidney, heart and lung tissues. However, PRLR mRNA levels
were increased in the thymus and no changes were observed in the spleen. The proportion
of transcripts for the different receptor isoforms (long, S1, S2 and S3) in liver and thymus
was not altered by LPS-injection. These findings suggest a complex tissue-specific
regulation of PRLR expression in the context of the APR.
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