GABA increases susceptibility to DSS-induced colitis in mice.

[Display omitted] • GABA fails to induce significant colitis within colons of healthy mice. • GABA facilitates susceptibility to DSS-induced colitis and impairs the intestinal barrier. • GABA inhibits colonic epithelium proliferation and promotes its apoptosis. Gamma-aminobutyric acid (GABA) is an important inhibitory neurotransmitter. Recently, it is considered to be a bioactive molecule with various health benefits. Ulcerative colitis (UC) is a chronic inflammatory disorder. An intestinal barrier defect is considered as one of the key events in the pathogenesis of UC. However, the issue of whether GABA is involved with intestinal inflammation remains debatable. In the present study, we investigated the effects of GABA on intestinal barrier function in healthy mice and susceptibility to UC in a dextran sulphate sodium (DSS) mouse model. Our results indicate that GABA treatment fails to induce significant colitis in healthy mice, however, GABA treatment enhances susceptibility to DSS-induced colitis in mice. Further, our results revealed GABA induces an intestinal barrier defect by inhibiting colonic epithelium proliferation and promoting its apoptosis. Accordingly, use of GABA treatment as applied for human health requires careful consideration. [ABSTRACT FROM AUTHOR]