GABA increases susceptibility to DSS-induced colitis in mice

Abstract

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.

Keywords

• Ulcerative colitis
• Gamma-aminobutyric acid
• Intestinal barrier
• Apoptosis
• Proliferation
• Junctional adhesion molecule 1