Molecular Modulation of Intestinal Epithelial Barrier: Contribution of Microbiota
Figure 3
Under normal physiological conditions, mucin secretion occurring at a stable rate (A) with signals from stable (commensal) microbiota. Mucin secretion is accelerated (B) upon activation by pathogenic organisms. In gram negative bacteria (e.g., Pseudomonas aeruginosa), both LPS (lipopolyscaccharide) and flagellin signal activation of RAS-MEK1/2-ERK1/2 (reticulo-activating system-pathway—meiosis-specific serine/threonine protein kinase-extracellular signal-regulated kinase) pathways. Bound to LPS binding protein (LBP), LPS uses a toll-like receptor (TLR). Flagellin binds to a glycolipid receptor, Asialo-GM1, which is calcium dependent. Lipoteichoic acid (LTA), a component of gram positive bacteria, binds to platelet activating factor (PAF) and activates ADAM10 (adhesion and protease domain molecule) which engages RAS/RAF/MEK/ERK/pp90RSK/NFB and MUC2 (intestinal mucin) production.
