title: Tissue-specific gene expression of prolactin receptor in the acute-phase response induced by lipopolysaccharides.
abstract: Acute inflammation can elicit a defense reaction known as the acute-phase response (APR) that is crucial for reestablishing 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 proinflammatory cytokines characteristic of the APR (TNF-alpha, IL-1beta, and IFNgamma) 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 downregulated in hepatic tissues after intraperitoneal LPS injection. Downregulation 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.
authors.affiliation: Division of Pulmonary and Critical Care Medicine, University of California, Davis 95616, USA. amcorbacho@ucdavis.edu
authors.forename: Ana M
authors.initials: AM
authors.lastname: Corbacho
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Valacchi
authors.forename: Lukas
authors.initials: L
authors.lastname: Kubala
authors.forename: Estibaliz
authors.initials: E
authors.lastname: Olano-Martín
authors.forename: Bettina C
authors.initials: BC
authors.lastname: Schock
authors.forename: Thomas P
authors.initials: TP
authors.lastname: Kenny
authors.forename: Carroll E
authors.initials: CE
authors.lastname: Cross
mesh_terms: D000210:Acute-Phase Reaction / Q000139:chemically induced / Q000378:metabolism*; D000818:Animals; D015153:Blotting, Western; D005786:Gene Expression Regulation / Q000502:physiology*; D007150:Immunohistochemistry; D007249:Inflammation / Q000139:chemically induced / Q000473:pathology; D007371:Interferon-gamma / Q000097:blood; D007375:Interleukin-1 / Q000097:blood; D008070:Lipopolysaccharides; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D011388:Prolactin / Q000097:blood; D012333:RNA, Messenger / Q000032:analysis / Q000096:biosynthesis; D011981:Receptors, Prolactin / Q000096:biosynthesis* / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013154:Spleen / Q000378:metabolism; D013950:Thymus Gland / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D007375:Interleukin-1; D008070:Lipopolysaccharides; D012333:RNA, Messenger; D011981:Receptors, Prolactin; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma; D011388:Prolactin