title: NF kappa B activation in mouse pituitary: comparison of response to interleukin-1 beta and lipopolysaccharide.
abstract: The mouse anterior pituitary contains both types of interleukin (IL)-1 receptors, IL-1 receptor type I (IL-1RI) and IL-1 receptor type II (IL-1RII). These receptors are expressed mainly on somatotroph cells. In the present study, the ability of the mouse pituitary to respond in vivo to IL-1 or to lipopolysaccharide (LPS) was demonstrated by measuring, with an electrophoretic mobility shift assay, the presence of an active NF kappa B complex in cell nuclei from pituitaries of mice injected intraperitoneally with recombinant rat-IL-1 beta or LPS. Using immunohistochemistry with an antibody directed against the p65 NF kappa B subunit, a rapid and transient NF kappa B response to LPS was observed. This response was present predominantly in the nuclei of glial fibrillary acidic protein (GFAP)-positive cells and F4/80-labelled cells of the posterior and the anterior pituitary 15 min after stimulation and became faint after 2 h. In comparison, the early and strong NF kappa B response to IL-1 beta treatment was localized into somatotroph cells, GFAP positive cells and F4/80-labelled cells of the posterior and anterior pituitary. Activation of NF kappa B in response to IL-1 beta was no longer apparent in IL-1RI knockout mice, confirming that this receptor is essential for the transduction of IL-1 signal in the pituitary, but remained after LPS treatment. In addition, we investigated the effect of IL-1 on target genes by measuring the mRNA and proteins synthesis of growth hormone (GH), IL-6 and IL-1ra in the pituitary and the plasma. IL-1 beta was shown to induce a rapid and strong synthesis of IL-6 and IL-1ra in the pituitary but failed to regulate GH contents or release. These data suggest that the pituitary is able to respond to a systemic infection via cytokine-mediated responses transduced by IL-1.
authors.affiliation: INRA-INSERM U394, Bordeaux, France. patricia.parnet@bordeaux.inserm.fr
authors.forename: P
authors.initials: P
authors.lastname: Parnet
authors.forename: F
authors.initials: F
authors.lastname: Pousset
authors.forename: S
authors.initials: S
authors.lastname: Laye
mesh_terms: D000818:Animals; D004247:DNA / Q000378:metabolism; D013006:Growth Hormone / Q000097:blood / Q000235:genetics; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1 / Q000494:pharmacology*; D015850:Interleukin-6 / Q000097:blood / Q000235:genetics; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008264:Macrophages / Q000378:metabolism; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D008817:Mice, Mutant Strains; D016328:NF-kappa B / Q000378:metabolism*; D010903:Pituitary Gland, Anterior / Q000187:drug effects / Q000378:metabolism*; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017472:Receptors, Interleukin-1 / Q000235:genetics; D053573:Receptors, Interleukin-1 Type I; D012795:Sialoglycoproteins / Q000235:genetics
chemical_list: C507764:Il1rn protein, mouse; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D015850:Interleukin-6; D008070:Lipopolysaccharides; D016328:NF-kappa B; D012333:RNA, Messenger; D017472:Receptors, Interleukin-1; D053573:Receptors, Interleukin-1 Type I; D012795:Sialoglycoproteins; D013006:Growth Hormone; D004247:DNA