Abstract
The intestinal microbiome maintains a close relationship with the host immunity. This connection fosters a health state by direct and indirect mechanisms. Direct influences occur mainly through the production of short-chain fatty acids (SCFAs), gastrointestinal hormones and precursors of bioactive molecules. Indirect mechanisms comprise the crosstalk between bacterial products and the host's innate immune system. Conversely, intestinal dysbiosis is a condition found in a large number of chronic intestinal inflammatory diseases, such as ulcerative colitis and Crohn's disease, as well as in diseases associated with low-grade inflammation, such as obesity, type 1 and 2 diabetes mellitus and cardiovascular diseases. NOD-Like receptors (NLRs) are cytoplasmic receptors expressed by adaptive and innate immune cells that form a multiprotein complex, termed the inflammasome, responsible for the release of mature interleukin (IL)-1β and IL-18. NLRs are also involved in the recognition of bacterial components and production of antimicrobial molecules that shape the gut microbiota and maintain the intestinal homeostasis. Recent novel findings show that NLRs may act as positive or negative regulators of inflammation by modulating NF-κB activation. This mini-review presents current and updated evidence on the interplay between NLRs and gut microbiota and their dual role, contributing to progression or conferring protection, in diabetes and other inflammatory diseases.
Highlights
The healthy human intestine is colonized by several microorganisms, including fungi, viruses, and bacteria belonging to different families [1]
Our results demonstrate that gut microbiota recognition by NOD2 in the pancreatic lymph nodes (PLNs) triggers a proinflammatory response, which induces a Th1 and Th17 cell pathogenic immune response, contributing to STZ-induced type 1 diabetes (T1D) pathogenesis (Table 1) [85]
Gut microbiota translocation to PLNs triggers proinflammatory response mediated by NOD2 activation, which contributes to STZ-induced T1D onset; Nod2-deficient non-obese diabetic (NOD) mice are protected from diabetes development and the protection is most likely mediated by altered gut microbiota
Summary
The healthy human intestine is colonized by several microorganisms, including fungi, viruses, and bacteria belonging to different families [1]. In models of type 2 diabetes (T2D), gut dysbiosis aggravates the inflammatory process, increases intestinal permeability and alters the metabolism of short-chain fatty acids, which are important in insulin resistance [56], in addition to accelerating the development of obesity, retinopathy and nephropathy [57].
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