Adiponectin is required for enhancement of CCL2 expression in adipose tissue during Listeria monocytogenes infection.
Adiponectin is required for enhancement of CCL2 expression in adipose tissue during Listeria monocytogenes infection.
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DOI：
10.1016/j.cyto.2009.12.005
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发表时间：
2010-05
期刊：
影响因子：
3.8
通讯作者：
H. Sashinami;A. Nakane
中科院分区：
文献类型：
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作者：
H. Sashinami;A. Nakane
肥胖是代谢综合征进展的重要背景。我们以前的研究表明，趋化因子CCL 2的表达被抑制的肥胖小鼠的肝脏，是非常容易感染李斯特菌。我们研究了脂联素在L.单核细胞增多症瘦素缺陷型肥胖ob/ob小鼠腹腔感染L.单核细胞增多症，消除细菌从脾脏，肝脏，肠系膜淋巴结和脂肪组织的抑制ob/ob小鼠相比，其杂合子同窝，ob/？小鼠CCL 2在ob/？L.单核细胞增多症感染，不同于ob/ob小鼠。类似地，在ob/ob小鼠的脂肪组织中未观察到脂联素表达。小鼠脂肪细胞3 T3-F442 A来源的脂肪细胞感染L.在单核细胞增多症中，在脂联素表达上调之后，CCL 2表达瞬时上调。L.通过敲低脂联素表达和补充重组脂联素部分恢复CCL 2表达来抑制单核细胞增多症感染。这些结果表明，脂联素是必要的适当表达的CCL 2，这是重要的巨噬细胞招募响应细菌感染。
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.