BACKGROUND: Cytokines mediate the metabolic and physiologic responses to injury and infection. Anterior pituitary cells express receptors for tumor necrosis factor (TNF) and interleukin 1 (IL-1), which can signal these cells to release corticotropin, growth hormone, and cytokines such as IL-1 and macrophage migration inhibitory factor. This interaction provides an important link between the immune system and the neuroendocrine system. We reasoned that pituicytes activated with TNF or IL-1 might release previously unrecognized factors that could participate in this signaling from the neuroendocrine to the immune system. METHODS: Proteins released from rat pituicytes (GH3) after stimulation with proinflammatory cytokines were identified by N-terminal amino acid sequencing. Polyclonal antibodies against a peptide corresponding to the N-terminal amino acid sequence were generated and used to determine the kinetics of protein release. RESULTS: Cytokine stimulation induced the release of a 30-kd protein from rat pituicytes. After the protein was isolated and the N-terminal amino acid sequence determined, a protein database analysis revealed that it is high mobility group-1 (HMG-1) protein. TNF and IL-1 induced the release of HMG-1 from pituicytes in a time- and dose-dependent manner. Interferon gamma alone did not induce the release of HMG-1, but it enhanced TNF-induced HMG-1 release. CONCLUSION: Stimulation of pituicytes by TNF or IL-1 induces the release of HMG-1, which may participate in the regulation of neuroendocrine and immune responses to infection or injury.
BACKGROUND: Cytokines mediate the metabolic and physiologic responses to injury and infection. Anterior pituitary cells express receptors for tumor necrosis factor (TNF) and interleukin 1 (IL-1), which can signal these cells to release corticotropin, growth hormone, and cytokines such as IL-1 and macrophage migration inhibitory factor. This interaction provides an important link between the immune system and the neuroendocrine system. We reasoned that pituicytes activated with TNF or IL-1 might release previously unrecognized factors that could participate in this signaling from the neuroendocrine to the immune system. METHODS: Proteins released from rat pituicytes (GH3) after stimulation with proinflammatory cytokines were identified by N-terminal amino acid sequencing. Polyclonal antibodies against a peptide corresponding to the N-terminal amino acid sequence were generated and used to determine the kinetics of protein release. RESULTS: Cytokine stimulation induced the release of a 30-kd protein from rat pituicytes. After the protein was isolated and the N-terminal amino acid sequence determined, a protein database analysis revealed that it is high mobility group-1 (HMG-1) protein. TNF and IL-1 induced the release of HMG-1 from pituicytes in a time- and dose-dependent manner. Interferon gamma alone did not induce the release of HMG-1, but it enhanced TNF-induced HMG-1 release. CONCLUSION: Stimulation of pituicytes by TNF or IL-1 induces the release of HMG-1, which may participate in the regulation of neuroendocrine and immune responses to infection or injury.
Authors: S Müller; P Scaffidi; B Degryse; T Bonaldi; L Ronfani; A Agresti; M Beltrame; M E Bianchi Journal: EMBO J Date: 2001-08-15 Impact factor: 11.598
Authors: B Sparatore; M Patrone; M Passalacqua; M Pedrazzi; D Gaggero; S Pontremoli; E Melloni Journal: Biochem J Date: 2001-07-15 Impact factor: 3.857
Authors: Luis Ulloa; Mahendar Ochani; Huan Yang; Mahira Tanovic; Daniel Halperin; Runkuan Yang; Christopher J Czura; Mitchell P Fink; Kevin J Tracey Journal: Proc Natl Acad Sci U S A Date: 2002-09-03 Impact factor: 11.205