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.