Lactobacillus acidophilus PIN7 paraprobiotic supplementation ameliorates DSS-induced colitis through anti-inflammatory and immune regulatory effects.

Abstract

This study aimed to evaluate the efficacy of paraprobiotics Lactobacillus acidophilus PIN7 supplementation against dextran sodium sulphate (DSS)-induced colitis in mice and to determine their mechanisms of the action. Ten-week-old female BALB/C mice were randomly divided into five groups. Each group was administered with PBS (control and DSS group), live PIN7 (LIVE group), heat-killed PIN7 (HEAT group) or lysozyme-treated PIN7 (LYSOZYME group) for 10days followed by 2.5% DSS supply in drinking water for 5days except for the control group. Colitis-associated DAI scores were significantly (p<0.05) attenuated in HEAT and LYSOZYME group. The HEAT group exhibited significantly (p<0.05) lower colonic tissue damage score compared to the DSS group. Furthermore, HEAT and LYSOZYME groups showed significantly (p<0.05) higher colonic expressions of toll-like receptor (TLR) 6 and intestinal junction protein E-cadherin and occludin compared to the DSS group. LYSOZYME group showed significantly (p<0.05) lower colonic expressions of Th2 cell-associated pro-inflammatory molecules, namely GATA3 and IL-4, and higher expression of anti-inflammatory NLRP6 and IL-18 compared to the DSS group. Also, HEAT group exhibited significantly (p<0.05) lower colonic p-IκBα expression compared to the DSS group, while COX-2 expression was significantly (p<0.05) suppressed by both paraprobiotics supplementation. Paraprobiotics significantly altered the composition of the intestinal microbiota. Paraprobiotic L. acidophilus PIN7 ameliorated DSS-induced colitis by regulating immune-modulatory TLR6 signalling and gut microbiota composition. This study suggests paraprobiotic L. acidophilus PIN7 are superior candidates to prevent intestinal inflammation associated with dysregulated immune responses.