Fig. 2: Diagrammatic representation of the interaction between the immune system, mucus layer, epithelial barrier, and microbiota in a disease/dysbiotic gut environment. A. Impaired/degraded mucus layer, glycocalyx, and epithelial barrier grants access to both commensal and pathogenic/pathobiont bacteria to permeate beyond the barrier. A decreased amount of mucin-producing goblet cells and altered mucin glycosylation and sialylation lead to an impaired mucus layer and glycocalyx. Decreased fucosylation due to downregulated FUT2 activity or CD4+ T-cell pro-inflammatory IL-10 secretion impairs positive growth.B . IL-6 and TNF-⍺ secretions promote altered mucin glycosylation by modulating glycosyltransferase activity. C.CX3CR1hi mononuclear phagocytes transport commensal bacteria to CD103+ dendritic cells in the mesenteric lymph nodes, inducing pro-inflammatory T-cell responses and increased IgA production and aggregation.D. Downregulated Mincle levels and Mincle-dependent immune evasion by opportunistic pathobionts. E. DC-SIGN-dependent immune evasion enabled by Th1 pro-inflammatory response inhibition after recognition of pathogenic/pathobiont bacteria. F. Additional pro-inflammatory responses induce the inflammatory gut environment by Th17 cell activity, Siglec activity, immunogenic dendritic cells and macrophages, and galectin-3,-4, and -9 activity. G. Altered digestion of dietary and host glycans leads to altered production of monosaccharides, disaccharides, and SCFA.