Fig. 4

Gut microbiota and inflammatory bowel disease. Gut microbiota dysbiosis, characterized by alterations in microbial composition and function, is strongly associated with IBD. A decrease in beneficial bacteria like Firmicutes and an increase in harmful bacteria like Proteobacteria contribute to disrupted intestinal barrier function and inflammation. Additionally, reduced short-chain fatty acid production and increased sulfate-reducing bacteria further exacerbate the inflammatory response. Genetic factors also play a significant role in IBD pathogenesis. Mutations in genes such as NOD2, ATG16L1, CARD9, and CLEC7A impair the immune response and enhance susceptibility to IBD. For instance, NOD2 mutations are linked to decreased IL-10 production and increased mucosal bacterial colonization. Moreover, the interaction between NOD2 and ATG16L1 is crucial for bacterial clearance and antigen presentation. Disruptions in this interaction, caused by mutations in either gene, can lead to increased pro-inflammatory cytokine secretion and exacerbated gut inflammation. ATG16L1, autophagy-related 16-like 1; CARD9, caspase recruitment domain-containing protein 9; CLEC7A, C-type lectin domain family 7 member A; IBD, inflammatory bowel disease; IL, interleukin; NOD2, nucleotide-binding and oligomerization domain 2 gene; SCFAs, short-chain fatty acids