Obesity is a chronic low-grade inflammatory condition, with increased inflammatory mediators in the circulation and adipose tissue. Following up obese subjects before and after bariatric surgery, we observed a biphasic regulation of pro-inflammatory factors in circulation, showing drastic decreases at month 3 post-surgery followed by a rebound and stabilization after 1 year. Patient's nutritional status was a major determinant of this unexpected profile. In obese subjects, we found enrichment in "non-classical" CD14dimCD16+ circulating monocytes that was reduced after bariatric surgery. The pathogenicity of this particular subset in relation with low-grade inflammation remains to be established. Although obese adipose tissue is a site of immune cell infiltration in obesity, little is known about cross-talk between these cell types. We show that adipose tissue macrophages secrete IL-1β through NLRP3 inflammasome activation. This process was down-regulated by weight loss but overactivated in type 2 diabetic (T2D) patients. We also showed that the adipose tissue of obese T2D subjects is enriched in IL-17+IFN-β+ double producer lymphocytes. In primary cell co-culture experiments, adipose tissue macrophage-derived IL-1β enhanced IL-17 production by adipose tissue lymphocytes, while IL-17 reciprocally induced IL-1β secretion. T2D might exacerbate this cross-talk, as suggested by overexpression of each cytokine cognate receptor on their respective target cell. This identified IL-1β and IL-17 as two key cytokines mediating a new inflammatory cross-talk between adipose tissue macrophages and lymphocytes that might contribute to the deterioration of glycemic status in human obesity
