Figure 1.

Working model of factors contributing to increased bacterial translocation and adipose tissue activation in Crohn’s disease. Alterations in mucus and at the cellular level of the intestinal barrier all contribute to increased translocation of bacterial cells. Bacteria and microbe-associated molecular patterns reach adipose tissue where the subsequent stimulation of pattern recognition receptors affects the ballance of cytokines and adipokines released at this site. In consequence macrophages are recruited and polarized either toward a pro-inflammatory M1 phenotype (e.g., in the lamina propria, orange color) or a regulatory M2 phenotype (e.g., in the mesenteric fat, blue color).