Pini Maria, Gove Melissa E, Sennello Joseph A, van Baal Jantine W P M, Chan Lawrence, Fantuzzi Giamila
Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois 60612, USA.
Endocrinology. 2008 Aug;149(8):4080-5. doi: 10.1210/en.2008-0327. Epub 2008 May 1.
Adipokines, cytokines mainly produced by adipocytes, are active participants in the regulation of inflammation. Administration of zymosan (ZY) was used to investigate the regulation and role of adipokines during peritonitis in mice. Injection of ZY led to a significant increase in leptin levels in both serum and peritoneal lavage fluid, whereas a differential trend in local vs. systemic levels was observed for both resistin and adiponectin. The role of leptin in ZY-induced peritonitis was investigated using leptin-deficient ob/ob mice, with and without reconstitution with exogenous leptin. Leptin deficiency was associated with delayed resolution of peritoneal inflammation induced by ZY, because ob/ob mice had a more pronounced cellular infiltrate in the peritoneum as well as higher and prolonged local and systemic levels of IL-6, TNFalpha, IL-10, and chemokine (C-X-C motif) ligand 2 compared with wild-type mice. Reconstitution with exogenous leptin exacerbated the inflammatory infiltrate and systemic IL-6 levels in ob/ob mice while inhibiting production of TNFalpha, IL-10, and chemokine (C-X-C motif) ligand 2. In contrast with the important role of leptin in regulating each aspect of ZY-induced peritonitis, adiponectin deficiency was associated only with a decreased inflammatory infiltrate, without affecting cytokine levels. These findings point to a complex role for adipokines in ZY-induced peritonitis and further emphasize the interplay between obesity and inflammation.
脂肪因子主要由脂肪细胞产生，是炎症调节的积极参与者。使用酵母聚糖（ZY）给药来研究脂肪因子在小鼠腹膜炎期间的调节作用和作用。注射ZY导致血清和腹腔灌洗液中瘦素水平显著升高，而抵抗素和脂联素在局部与全身水平呈现不同趋势。使用瘦素缺乏的ob/ob小鼠，在有或没有外源性瘦素重建的情况下，研究瘦素在ZY诱导的腹膜炎中的作用。瘦素缺乏与ZY诱导的腹膜炎炎症消退延迟有关，因为与野生型小鼠相比，ob/ob小鼠腹膜中有更明显的细胞浸润，以及局部和全身的IL-6、TNFα、IL-10和趋化因子（C-X-C基序）配体2水平更高且持续时间更长。用外源性瘦素重建会加剧ob/ob小鼠的炎症浸润和全身IL-6水平，同时抑制TNFα、IL-10和趋化因子（C-X-C基序）配体2的产生。与瘦素在调节ZY诱导的腹膜炎各个方面的重要作用相反，脂联素缺乏仅与炎症浸润减少有关，而不影响细胞因子水平。这些发现表明脂肪因子在ZY诱导的腹膜炎中具有复杂的作用，并进一步强调了肥胖与炎症之间的相互作用。
