Absence of NOD2 receptor predisposes to intestinal inflammation by a deregulation in the immune response in hosts that are unable to control gut dysbiosis

NOD2 Deficiency Promotes Intestinal CD4+ T Lymphocyte Imbalance, Metainflammation, and Aggravates Type 2 Diabetes in Murine Model

“…In accordance, NOD2 −/− mice have decreased number and impaired activation of Th17 cells in the gut after exposure to C. rodentium and Salmonella spp. (38,39). Additionally, activation of NOD2 receptors by MDP promotes Th17 cells differentiation and activation (40,41).…”

Editorial: Intestinal Dysbiosis in Inflammatory Diseases

“…These molecules can bind specific receptors on mucosal cells and impact the local or systemic immunity, by inducing regulatory T cells (Tregs) and an antiinflammatory response that control the exacerbated reactions in the gut mucosa, thus contributing to the maintenance of the barrier integrity (14,15). Moreover, epithelial or mucosal immune cells express pattern recognition receptors (Toll-like receptors -TLRs, NOD-like receptors -NLRs, and others) that also contribute to the sensing of the host microbiota and regulation of inflammatory processes (16). Interestingly, on this Research Topic, Elias-Oliveira et al emphasized the interactions between NLRs and gut microbiota, showing the dual role of these molecules in promoting inflammation or protecting against the harmful effects of dysbiosis-driven diseases, such as IBD, type 1 or type 2 diabetes and obesity.…”

NLR and Intestinal Dysbiosis-Associated Inflammatory Illness: Drivers or Dampers?

“…NOD2 is an innate immunity receptor that recognizes peptidoglycan in the cell wall of bacteria and, therefore, constitutes an important link between gut microbiota and immunity (116). Therefore, NOD2 activation profile may be important in metabolic diseases with immune branches and, therefore, may represent the link in the cross-talk between the gut microbiota and these diseases.…”

“…Therefore, NOD2 activation profile may be important in metabolic diseases with immune branches and, therefore, may represent the link in the cross-talk between the gut microbiota and these diseases. The deficiency of NOD2 in mice allows greater translocation of bacteria from the intestine (116). In a model of HFD, mice deficient in NOD2 exhibit greater peripheral resistance to insulin, inflammation of visceral adipose tissue, and higher content of bacterial DNA in the liver (117).…”