Department of Microbiology and Immunology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Cytokine. 2010 May;50(2):170-4. doi: 10.1016/j.cyto.2009.12.005. Epub 2009 Dec 31.
Obesity is an important background of metabolic syndrome progression. Our previous study demonstrated that chemokine CCL2 expression was suppressed in liver of obese mice that were highly susceptible to Listeria monocytogenes infection. We investigated the role of adiponectin in CCL2 expression in obese mice after L. monocytogenes infection. When leptin-deficient obese ob/ob mice were infected intraperitoneally with L. monocytogenes, the elimination of bacteria from spleen, liver, mesenteric lymph nodes and adipose tissue was inhibited in ob/ob mice compared with their heterozygote littermates, ob/? mice. CCL2 expression in the adipose tissue of ob/? mice was enhanced by L. monocytogenes infection, different from ob/ob mice. Similarly, adiponectin expression was not observed in the adipose tissue of ob/ob mice. When mouse adipocyte 3T3-F442A-derived adipocytes were infected with L. monocytogenes, CCL2 expression was transiently up-regulated, following up-regulation of adiponectin expression. Up-regulation of CCL2 in adipocytes by L. monocytogenes infection was suppressed by knocked-down of adiponectin expression and supplementation of recombinant adiponectin partially recovered CCL2 expression. These results suggest that adiponectin is required for appropriate expression of CCL2 that is important for macrophage recruitment in response to bacterial infection.
肥胖是代谢综合征进展的重要背景。我们之前的研究表明，趋化因子 CCL2 的表达在易感染李斯特菌的肥胖小鼠的肝脏中受到抑制。我们研究了在肥胖小鼠感染李斯特菌后脂联素在 CCL2 表达中的作用。当瘦素缺乏的肥胖 ob/ob 小鼠经腹腔感染李斯特菌时，与杂合子 littermates ob/? 小鼠相比，ob/ob 小鼠脾脏、肝脏、肠系膜淋巴结和脂肪组织中的细菌清除受到抑制。ob/? 小鼠的脂肪组织中 CCL2 的表达因李斯特菌感染而增强，与 ob/ob 小鼠不同。同样，ob/ob 小鼠的脂肪组织中没有观察到脂联素的表达。当用李斯特菌感染小鼠脂肪细胞 3T3-F442A 衍生的脂肪细胞时，脂联素表达先上调，随后 CCL2 表达短暂上调。L. monocytogenes 感染对脂肪细胞中 CCL2 的上调作用被脂联素表达下调所抑制，而重组脂联素的补充部分恢复了 CCL2 的表达。这些结果表明，脂联素是适当表达 CCL2 所必需的，CCL2 对细菌感染时巨噬细胞的募集很重要。
