| First Author | Zhang Y | Year | 2015 |
| Journal | Immunity | Volume | 42 |
| Issue | 5 | Pages | 953-964 |
| PubMed ID | 25992864 | Mgi Jnum | J:229739 |
| Mgi Id | MGI:5754413 | Doi | 10.1016/j.immuni.2015.04.016 |
| Citation | Zhang Y, et al. (2015) Epidermal Fatty Acid binding protein promotes skin inflammation induced by high-fat diet. Immunity 42(5):953-64 |
| abstractText | Defining specific cellular and molecular mechanisms in most obesity-related diseases remains an important challenge. Here we report a serendipitous finding that consumption of a high-fat diet (HFD) greatly increased the occurrence of skin lesions in C57BL/6 mice. We demonstrated that HFD induced the accumulation of a specific type of CD11c(+) macrophages in skin preceding detectable lesions. These cells primed skin to induce IL-1beta and IL-18 signaling, which further promoted the cytokines IFN-gamma- and IL-17-mediated skin inflammation. Mechanistically, epidermal fatty acid binding protein (E-FABP) was significantly upregulated in skin of obese mice, which coupled lipid droplet formation and NLRP3 inflammasome activation. Deficiency of E-FABP in obese mice decreased recruitment of CD11c(+) macrophages in skin tissues, reduced production of IL-1beta and IL-18, and consequently dampened activation of effector T cells. Furthermore, E-FABP-deficient mice are completely resistant to HFD-induced skin lesions. Collectively, E-FABP represents a molecular sensor triggering HFD-induced skin inflammation. |
