Surface-layer protein from Lactobacillus acidophilus NCFM attenuates tumor necrosis factor-α-induced intestinal barrier dysfunction and inflammation.

Abstract

Lactobacillus acidophilus NCFM, a probiotic generally regarded as safe, carries a proteinaceous surface (S) layer, composed of numerous identical subunits (surface layer protein, Slp). S-layer proteins have been confirmed to possess multiple biological properties, but their role in maintaining the intestinal epithelial barrier is not fully known. We investigated the effects of Slp on tumor necrosis factor (TNF)-α-elicited intestinal barrier dysfunction and explored the underlying molecular mechanism. TNF-α administration markedly induced intestinal epithelial injury and inflammation in Caco-2 cells. Preincubation of Caco-2 cells with Slp at concentrations ranging from 50 to 100 μg/mL for 6 h improved intestinal epithelial cell integrity and permeability, restored ZO-1 and Occludin protein expressions (P < 0.05) and reduced the secretion of interleukin 8 by a maximum of 47.8%. Furthermore, the addition of Slp to Caco-2 cell monolayers attenuated cell apoptosis and inhibited nuclear factor-κB (NF-κB) p65 nucleus translocation by suppressing the activation of NF-κB. Collectively, the ability of Slp to attenuate dysfunction of the intestinal epithelial barrier stimulated by TNF-α and to exert anti-inflammatory effects supports its potential use in the development of functional foods and in the prevention of inflammatory bowel diseases.

Keywords: Caco-2 cell monolayers; Inflammation; Intestinal epithelial barrier; L. acidophilus NCFM; Surface-layer protein.