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植物乳杆菌可预防实验性结肠炎模型中黏附分子表达的上调。

Lactobacillus plantarum prevents the upregulation of adhesion molecule expression in an experimental colitis model.

机构信息

Department of Surgery, The Sixth People's Hospital Affiliated to Shanghai Jiao Tong University, 600 Yishan Road, 200233, Shanghai, China.

出版信息

Dig Dis Sci. 2010 Sep;55(9):2505-13. doi: 10.1007/s10620-009-1063-2. Epub 2009 Dec 4.

DOI:10.1007/s10620-009-1063-2
PMID:19960256
Abstract

BACKGROUND

Lactobacillus consumption has been shown to attenuate the severity of experimental colitis. Whether the effects of Lactobacillus on colitis are related to modulation of leukocyte recruitment into the inflamed intestine is unclear.

AIMS

To investigate the effect of Lactobacillus plantarum daily intragastric administration on lymphocyte homing and intestinal inflammation in interleukin 10 (IL-10) knockout mice, an experimental model of colitis.

METHODS

Two groups of ten IL-10 knockout mice were fed phosphate buffered saline containing Lactobacillus plantarum 1258 or unmodified vehicle for 4 weeks. Two groups of ten wild-type mice were used as controls. At killing, the bowels were histologically scored and evaluated by transmission electron microscopy. Mucosal addressin cell adhesion molecule 1 (MAdCAM-1) and intercellular adhesion molecule 1 (ICAM-1) expression were determined by immunohistochemistry. The levels of proinflammatory cytokines, tumor necrosis factor alpha (TNF-alpha), and interferon gamma (IFN-gamma) were determined by ELISA. In addition, levels of CD3, alpha4beta7, ICAM-1, and MAdCAM-1 were determined by reverse-transcription polymerase chain reaction and Western blot.

RESULTS

L. plantarum treatment improved the histological damage score in KO mice compared to untreated KO mice. L. plantarum significantly attenuated the expression of MAdCAM-1, ICAM-1, CD3, and alpha4beta7, but did not affect the levels of TNF-alpha and IFN-gamma when treated KO mice were compared to untreated KO mice.

CONCLUSIONS

L. plantarum interfered with the upregulation of adhesion molecules observed in IL-10 knockout mice compared to wild-type mice, attenuating the symptoms of colitis.

摘要

背景

已有研究表明,摄入乳酸菌可减轻实验性结肠炎的严重程度。然而,乳酸菌对结肠炎的影响是否与调节白细胞向炎症肠道募集有关尚不清楚。

目的

研究每日胃内给予植物乳杆菌对白细胞介素 10(IL-10)敲除小鼠结肠炎,即一种结肠炎实验模型,中淋巴细胞归巢和肠道炎症的影响。

方法

两组共 20 只 IL-10 敲除小鼠分别用含植物乳杆菌 1258 或未修饰载体的磷酸盐缓冲液喂养 4 周。两组共 20 只野生型小鼠作为对照。处死时,通过组织学评分和透射电镜评估肠道,并通过免疫组织化学测定粘膜地址素细胞黏附分子 1(MAdCAM-1)和细胞间黏附分子 1(ICAM-1)的表达。通过 ELISA 测定促炎细胞因子肿瘤坏死因子-α(TNF-α)和干扰素-γ(IFN-γ)的水平。此外,通过逆转录聚合酶链反应和 Western blot 测定 CD3、α4β7、ICAM-1 和 MAdCAM-1 的水平。

结果

与未治疗的 KO 小鼠相比,植物乳杆菌治疗可改善 KO 小鼠的组织学损伤评分。与未治疗的 KO 小鼠相比,植物乳杆菌治疗显著降低了 MAdCAM-1、ICAM-1、CD3 和 α4β7 的表达,但对 TNF-α和 IFN-γ的水平没有影响。

结论

与野生型小鼠相比,植物乳杆菌干预了 IL-10 敲除小鼠中观察到的粘附分子的上调,从而减轻了结肠炎的症状。

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