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.