By using special hydrogel beads to protect p40 from degradation, we showed that p40 reduced intestinal epithelial apoptosis and preserved barrier function in the colon epithelium in an EGF receptor-dependent manner, thereby preventing and treating intestinal inflammation in mouse models of colitis.
Experimental models of colitis highlighted that IL-9-producing T cells critically interfered with an intact barrier function of the intestinal epithelium by impacting cellular proliferation and tight junction molecules.
In addition, adoptive transfer of such IL-9-producing CD4<sup>+</sup> T helper cells was shown to cause the development of colitis and peripheral neuritis.
Importantly, the colonic epithelial cell-derived components potentiated LGG-produced p40 levels in a mouse model of colitis and enhanced LGG-mediated amelioration of intestinal inflammation in this model.