Figure 2
From: Gut permeability and mucosal inflammation: bad, good or context dependent
Alterations in tight junction proteins expression/cellular distribution may influence mucosal inflammatory conditions by modulating mucosal homeostasis and gut permeability. (a) Pathological (upregulated) expression of claudin-1 in mouse gut epithelium hyperactivates Notch-signaling to inhibit goblet cell/Mucin-2 synthesis, which in turn increases susceptibility to chronic inflammation. (b) Increased claudin-2 expression in mouse gut epithelium, similar to IBD patients, increases gut permeability and colonocyte proliferation. Presence of anergic macrophages and increased numbers of regulatory T cells (Treg cells) in the lamina propria of claudin-2 transgenic mice suggest immune compensation. As expected, these mice are resistant to experimentally induced colitis.
