Proinflammatory cytokines (tumor necrosis factor and interleukin 1) stimulate release of high mobility group protein-1 by pituicytes

• Published in: Surgery Vol. 126; no. 2; pp. 389 - 392
• Main Authors: Wang, Haichao, Vishnubhakat, Jaideep M., Bloom, Ona, Zhang, Minghuang, Ombrellino, Michael, Sama, Andrew, Tracey, Kevin J.
• Format: Journal Article Conference Proceeding
• Language: English
• Published: New York, NY Mosby, Inc 01.08.1999; Elsevier
• Subjects: Amino Acid Sequence; Animals; Biological and medical sciences; Carrier Proteins - secretion; Cell Line; High Mobility Group Proteins - secretion; HMGB1 Protein; Interferon-gamma - pharmacology; Interleukin-1 - pharmacology; Medical sciences; Miscellaneous; Molecular Sequence Data; Pituitary Gland - cytology; Pituitary Gland - drug effects; Pituitary Gland - secretion; Rats; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases; Tumor Necrosis Factor-alpha - pharmacology; Animal model; Endocrine gland; Rat; Interaction; Rodentia; Trauma; Infection; Vertebrata; Mammalia; Cell line; Tumor necrosis factor; Animal; Surgery; Interleukin 1; Pituicyte; Complication; Immune system
• ISSN: 0039-6060; 1532-7361
• DOI: 10.1016/S0039-6060(99)70182-0

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 (GH 3) 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. (Surgery 1999;126:389-92.)