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嗜热链球菌ST28通过抑制炎性Th17细胞部分改善小鼠结肠炎。

Streptococcus thermophilus ST28 ameliorates colitis in mice partially by suppression of inflammatory Th17 cells.

作者信息

Ogita Tasuku, Nakashima Megumi, Morita Hidetoshi, Saito Yasuo, Suzuki Takuya, Tanabe Soichi

机构信息

Graduate School of Biosphere Science, Hiroshima University, 1-4-4 Kagamiyama, Higashi-hiroshima, Hiroshima 739-8528, Japan.

出版信息

J Biomed Biotechnol. 2011;2011:378417. doi: 10.1155/2011/378417. Epub 2011 Oct 12.

DOI:10.1155/2011/378417
PMID:22013382
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3196311/
Abstract

The effects of Streptococcus thermophilus ST28 on cytokine production by murine splenocytes stimulated with transforming growth factor-β plus interleukin- (IL-) 6 were evaluated. The addition of ST28 significantly repressed IL-17 production compared to ATCC 19258 (type strain). ST28 also decreased the number of Th17 cells in the stimulated splenocytes. The anti-inflammatory effects of ST28 administration were evaluated in mice with colitis induced by dextran sodium sulphate (DSS). Oral treatment of mice with ST28 ameliorated the intestinal lesions by DSS. Upon DSS treatment, IL-17 production in lamina propria lymphocytes (LPLs) was induced, but ST28 significantly decreased its production. ST28 also decreased the percentage of Th17 cells in LPL from DSS-induced colitis. The present results imply that ST28 suppresses the Th17 response in inflamed intestines and would be useful in the treatment of Th17-mediated diseases, such as inflammatory bowel disease.

摘要

评估了嗜热链球菌ST28对用转化生长因子-β加白细胞介素-（IL-）6刺激的小鼠脾细胞产生细胞因子的影响。与ATCC 19258（模式菌株）相比，添加ST28显著抑制了IL-17的产生。ST28还减少了受刺激脾细胞中Th17细胞的数量。在葡聚糖硫酸钠（DSS）诱导的结肠炎小鼠中评估了ST28给药的抗炎作用。用ST28口服治疗小鼠可改善DSS引起的肠道损伤。在DSS治疗后，固有层淋巴细胞（LPL）中诱导了IL-17的产生，但ST28显著降低了其产生。ST28还降低了DSS诱导的结肠炎LPL中Th17细胞的百分比。目前的结果表明，ST28抑制炎症肠道中的Th17反应，对治疗Th17介导的疾病如炎症性肠病可能有用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b03/3196311/126a402df76d/JBB2011-378417.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b03/3196311/ee3a525746e5/JBB2011-378417.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b03/3196311/c0ed58cb7e04/JBB2011-378417.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b03/3196311/dfb808a3143f/JBB2011-378417.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b03/3196311/243cd9a93fe9/JBB2011-378417.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b03/3196311/126a402df76d/JBB2011-378417.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b03/3196311/ee3a525746e5/JBB2011-378417.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b03/3196311/c0ed58cb7e04/JBB2011-378417.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b03/3196311/dfb808a3143f/JBB2011-378417.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b03/3196311/243cd9a93fe9/JBB2011-378417.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b03/3196311/126a402df76d/JBB2011-378417.005.jpg

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