Immune mechanisms involved in obesity

Obesity is a widespread public health problem worldwide. This disease has been classified as a condition caused by excessive accumulation of triglycerides in adipose tissue (TA). Visceral TA is an important factor in the development of several chronic diseases, since the adipocyte increases in size and number, leading to hypoxia, fatty acid release, mobilization and activation of leukocyte subpopulations (macrophages, neutrophils, eosinophils, NK cells, T lymphocytes and B); release of pro-inflammatory mediators (TNF-a, IL-6, PAI-1, resistin and visfatin), and decreased secretion of anti-inflammatory cytokines (adiponectin, IL-10, IL-4 and IL-13). These changes in TAV generate a chronic inflammation state of low intensity, that has been linked to insulin resistance (IR), initially local and then becomes systemic, which represents the determining factor for the development of metabolic syndrome (SM). The transcendence of TAV in the interaction between adipose and immune cells, as well as the release of mediators that trigger the chronic inflammatory process, is key for the development of IR and SM. However, in the investigation of obesity and the development of its comorbidities, it has been observed that the skeletal-muscle mass is involved in this process, apart from the cells and mediators of which their participation is known. In this way, TCD4 and TCD8 lymphocytes are recognized as pro-inflammatory. In contrast, eosinophils and adiponectin are considered as protective of the process.