Systemic and intestinal chronic inflammation, diet and cancer: an unbreakable bond

Idiopathic intestinal inflammatory diseases (IID) include two types of chronic intestinal disorders: Crohn’s disease and ulcerative rectocolitis. Evidence suggests that the IID is derived from the loss of immune tolerance in normal enteric bacteria diners in a genetically susceptible host. In humans, the initial intestinal immune response to intestinal microbiota is closely regulated; this regulation determines if there is a condition of immune tolerance or an inflammatory defensive response. The alteration of the balance of this immune response can lead to IID. In healthy people, the intestinal lamina contains a complex population of cells of the immune system that secrete cytokines with the function of modulating the immune response, both in the anti-inflammatory direction that reduces immune response transforming growth factor β (TGF-β) and Interleukin-10 and pro-inflammatory direction. All these mediators are produced by innate and adaptive immune cells, which limit the excessive entry of intestinal microbiota and defend themselves from pathogens. The balance of the immune response is maintained between regulatory T cells and effector T cells (Th1, Th2, and Th17). In IID, innate cells increase the production of tumor necrosis factor-alpha (TNF-α), interleukin-1β, interleukin-6, interleukin-12, interleukin-23, and chemokines. There is a marked increase in the thickness of the lamina propria, with an increase in the number of CD4+ T cells, in particular proinflammatory subgroups of T cells, which also produce cytokines and chemokines in high quantities. This increase in the production of cytokines determines the recruitment of further leukocytes, thus determining a vicious circle that maintains the state of inflammation.