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The Leptin System: A Potential Target for Sepsis Induced Immune Suppression

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Sepsis, which is defined as a systemic inflammatory response syndrome that occurs during infection, is associated with several clinical conditions and high mortality rates. As sepsis progresses immune paralysis can become severe, leaving an already vulnerable patient ill equipped to eradicate primary or secondary infections. At present the predominant treatments for sepsis have not demonstrated convincing efficacy of decreased mortality. During sepsis, it has been observed that leptin levels initially increase but subsequently decline. A body of evidence has demonstrated that central or systemic leptin can beneficially regulate immune function. In this report expression of leptin and its receptor, signaling, and function on leukocytes will be reviewed. Furthermore, the effects mediated by central and systemic leptin during sepsis will be reviewed. Altogether, the ability of leptin to beneficially enhance inflammation and the host response during sepsis supports its use as a therapeutic agent, particularly during the latter phases of the syndrome.





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Keywords: 3-phosphatidylinositol; 5-adenosine monophosphate-activated protein kinase; ANS; G-CSF receptor; HPA; Leptin; Protein tyrosine phosphatase 1B; SNS; T cell; Tyrosine Phosphorylation; anti-microbial; autonomic nervous system; choroid plexus; cytokine receptor homology; cytokine signaling 3; extracellular signaling pathway; hematopoiesis; hypothalamo-pituitary adrenocortical; hypothalamus; insulin receptor substrate; leptin protein receptor; macrophage; neutrophil; peripheral blood mononuclear cells; phosphatase 1B; pro-opiomelanocortin; rapamycin; sympathetic nervous system; thermogenesis; tumor necrosis factor alpha (TNF); ventromedial

Document Type: Research Article

Publication date: December 1, 2010

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  • This journal is devoted to timely reviews of experimental and clinical studies in the field of endocrine, metabolic, and immune disorders. Specific emphasis is placed on humoral and cellular targets for natural, synthetic, and genetically engineered drugs that enhance or impair endocrine, metabolic, and immune parameters and functions. Topics related to the neuroendocrine-immune axis are given special emphasis in view of the growing interest in stress-related, inflammatory, autoimmune, and degenerative disorders.
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