BioAcyl Corp
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Dixit, V. D., Schaffer, E. M., & Pyle, R. S. (2004). Ghrelin inhibits leptin- and activation-induced proinflammatory cytokine expression by human monocytes and T cells. The Journal of Clinical Investigation, 114(1), 57–66. Added by: Dr. Enrique Feoli (14/10/2023, 18:36) Last edited by: Dr. Enrique Feoli (14/10/2023, 18:37) |
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| Resource type: Journal Article DOI: 10.1172/JCI21134 BibTeX citation key: Dixit2004 View all bibliographic details  |
Categories: BioAcyl Corp Subcategories: Analgesia Creators: Dixit, Pyle, Schaffer Collection: The Journal of Clinical Investigation |
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| Abstract |
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Ghrelin, a recently described endogenous ligand for the growth hormone secretagogue receptor (GHS-R), is produced by stomach cells and is a potent circulating orexigen, controlling energy expenditure, adiposity, and growth hormone secretion. However, the functional role of ghrelin in regulation of immune responses remains undefined. Here we report that GHS-R and ghrelin are expressed in human T lymphocytes and monocytes, where ghrelin acts via GHS-R to specifically inhibit the expression of proinflammatory anorectic cytokines such as IL-1β, IL-6, and TNF-α. Ghrelin led to a dose-dependent inhibition of leptin-induced cytokine expression, while leptin upregulated GHS-R expression on human T lymphocytes. These data suggest the existence of a reciprocal regulatory network by which ghrelin and leptin control immune cell activation and inflammation. Moreover, ghrelin also exerts potent anti-inflammatory effects and attenuates endotoxin-induced anorexia in a murine endotoxemia model. We believe this to be the first report demonstrating that ghrelin functions as a key signal, coupling the metabolic axis to the immune system, and supporting the potential use of ghrelin and GHS-R agonists in the management of disease-associated cachexia.
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| Notes |
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Publisher: The American Society for Clinical Investigation
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