R & D Center, Korea Yakult Co., Ltd., Yongin, Kyunggi-do 446-901, South Korea.
Inflammation. 2009 Dec;32(6):379-86. doi: 10.1007/s10753-009-9146-y.
To evaluate the anti-colitic effect of lactic acid bacteria by cDNA microarray analysis, a lactic acid bacteria mixture (LM) consisting of Lactobacillus brevis HY7401, L. suntoryeus HY7801 and Bifidobacterium longum HY8004 was orally administered to dextran sulfate (DSS)-induced colitic mice and the expression profile of numerous genes was assessed. DSS treatment caused colitic outcomes such as inflammation and colon shortening. DSS also up-regulated the expression of inflammation-related genes: pro-inflammatory and chemotactic cytokines, including IL-1beta, TNF-alpha, IL-6, CCL2, CCL4, CCL7, CCL24, CXCL1, CXCL2, CXCL5, CXCL9 and CXCL10, and their receptors CCR3 and CCR7, and other colitis-related genes such as COX-2, PAP, MMP family, S100a8, S100a9 and DEFA1. LM treatment inhibited the mRNA expression of inflammation-related and tissue remodeling genes induced by DSS as well as the colitic symptoms. LM inhibition for the DSS-induced expression of the representative inflammatory markers, IL-1beta, TNF-alpha and COX-2, was supported by quantitative real-time polymerase chain reaction analysis. These findings suggest that LM ameliorates DSS-induced colitis by regulating inflammatory-related cytokines as well as tissue remodeling genes.
为了通过 cDNA 微阵列分析评估乳酸菌的抗结肠炎症作用,将由短乳杆菌 HY7401、屎肠球菌 HY7801 和长双歧杆菌 HY8004 组成的乳酸菌混合物(LM)口服给予葡聚糖硫酸钠(DSS)诱导的结肠炎小鼠,并评估许多基因的表达谱。DSS 处理导致结肠炎结果,如炎症和结肠缩短。DSS 还上调了炎症相关基因的表达:促炎和趋化细胞因子,包括 IL-1β、TNF-α、IL-6、CCL2、CCL4、CCL7、CCL24、CXCL1、CXCL2、CXCL5、CXCL9 和 CXCL10,以及它们的受体 CCR3 和 CCR7,以及其他结肠炎相关基因,如 COX-2、PAP、MMP 家族、S100a8、S100a9 和 DEFA1。LM 处理抑制了 DSS 诱导的炎症相关和组织重塑基因的 mRNA 表达以及结肠炎症状。定量实时聚合酶链反应分析支持 LM 抑制 DSS 诱导的代表性炎症标志物 IL-1β、TNF-α 和 COX-2 的表达。这些发现表明,LM 通过调节炎症相关细胞因子以及组织重塑基因来改善 DSS 诱导的结肠炎。