溶菌酶
嗜酸乳杆菌
结肠炎
免疫系统
封堵器
免疫学
内科学
胃肠病学
化学
生物
益生菌
医学
细菌
生物化学
紧密连接
遗传学
作者
Yeon-Jin Kye,So‐Young Lee,Ha-Ra Kim,Byung‐Hoo Lee,Jong‐Hyun Park,Myeong-Soo Park,Geun Eog Ji,Mi‐Kyung Sung
摘要
Abstract Aims 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. Methods and Results 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 10 days followed by 2.5% DSS supply in drinking water for 5 days 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. Conclusion Paraprobiotic L. acidophilus PIN7 ameliorated DSS-induced colitis by regulating immune-modulatory TLR6 signalling and gut microbiota composition. Significance and Impact of the Study This study suggests paraprobiotic L. acidophilus PIN7 are superior candidates to prevent intestinal inflammation associated with dysregulated immune responses.
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