期刊
JOURNAL OF NEUROSCIENCE
卷 30, 期 17, 页码 6036-6047出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.4875-09.2010
关键词
-
资金
- National Institutes of Health [R01 GM72760]
- National Institute of Diabetes and Digestive and Kidney Diseases [59630, 69987, 56863]
- National Institute of Diabetes and Digestive and Kidney Diseases Obesity Center [PO1DK26687]
- Medical Research Council [G0900554] Funding Source: researchfish
- MRC [G0900554] Funding Source: UKRI
Sepsis describes a complex clinical syndrome that results from an infection, setting off a cascade of systemic inflammatory responses that can lead to multiple organ failure and death. Leptin is a 16 kDa adipokine that, among its multiple known effects, is involved in regulating immune function. Here we demonstrate that leptin deficiency in ob/ob mice leads to higher mortality and more severe organ damage in a standard model of sepsis in mice [cecal ligation and puncture (CLP)]. Moreover, systemic leptin replacement improved the immune response to CLP. Based on the molecular mechanisms of leptin regulation of energy metabolism and reproductive function, we hypothesized that leptin acts in the CNS to efficiently coordinate peripheral immune defense in sepsis. We now report that leptin signaling in the brain increases survival during sepsis in leptin-deficient as well as in wild-type mice and that endogenous CNS leptin action is required for an adequate systemic immune response. These findings reveal the existence of a relevant neuroendocrine control of systemic immune defense and suggest a possible therapeutic potential for leptin analogs in infectious disease.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据