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空肠弯曲杆菌暴露期间丁酸盐和鼠李糖乳杆菌GG对丁酸盐受体和转运蛋白的影响。

Effect of butyrate and Lactobacillus GG on a butyrate receptor and transporter during Campylobacter jejuni exposure.

作者信息

Cresci Gail A M, Mayor Paul C, Thompson Stuart A

机构信息

Pediatric Research Center, Department of Gastroenterology, Pediatrics Institute and Department of Pathobiology, Lerner Research Institute, Cleveland Clinic, OH 44195, USA.

Department of Gynecologic Oncology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA.

出版信息

FEMS Microbiol Lett. 2017 Mar 1;364(6). doi: 10.1093/femsle/fnx046.

DOI:10.1093/femsle/fnx046
PMID:28333199
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5399911/
Abstract

Campylobacter jejuni frequently infects humans causing many gastrointestinal symptoms, fever, fatigue and several long-term debilitating diseases. Current treatment for campylobacteriosis includes rehydration and in some cases, antibiotic therapy. Probiotics are used to treat several gastrointestinal diseases. Butyrate is a short-chain fatty acid known to promote intestinal health. Interaction of butyrate with its respective receptor (HCAR2) and transporter (SLC5A8), both expressed in the intestine, is associated with water and electrolyte absorption as well as providing defense against colon cancer and inflammation. Alterations in gut microbiota influence the presence of HCAR2 and SLC5A8 in the intestine. We hypothesized that adherence and/or invasion of C. jejuni and alterations in HCAR2 and SLC5A8 expression would be minimized with butyrate or Lactobacillus GG (LGG) pretreatment of Caco-2 cells. We found that both C. jejuni adhesion but not invasion was reduced with butyrate pretreatment. While LGG pretreatment did not prevent C. jejuni adhesion, it did result in reduced invasion which was associated with altered cell supernate pH. Both butyrate and LGG protected HCAR2 and SLC5A8 protein expression following C. jejuni infection. These results suggest that the first stages of C. jejuni infection of Caco-2 cells may be minimized by LGG and butyrate pretreatment.

摘要

空肠弯曲菌经常感染人类,导致许多胃肠道症状、发热、疲劳以及几种长期使人衰弱的疾病。目前弯曲菌病的治疗方法包括补液,在某些情况下还包括抗生素治疗。益生菌用于治疗多种胃肠道疾病。丁酸盐是一种已知能促进肠道健康的短链脂肪酸。丁酸盐与其在肠道中均有表达的相应受体(HCAR2)和转运体(SLC5A8)的相互作用,与水和电解质吸收相关,同时还能抵御结肠癌和炎症。肠道微生物群的改变会影响HCAR2和SLC5A8在肠道中的存在。我们假设,用丁酸盐或鼠李糖乳杆菌GG(LGG)预处理Caco-2细胞,可使空肠弯曲菌的黏附和/或侵袭以及HCAR2和SLC5A8表达的改变降至最低。我们发现,丁酸盐预处理可降低空肠弯曲菌的黏附,但不会降低其侵袭。虽然LGG预处理不能阻止空肠弯曲菌的黏附,但确实能减少其侵袭,这与细胞上清液pH值的改变有关。丁酸盐和LGG在空肠弯曲菌感染后均能保护HCAR2和SLC5A8的蛋白表达。这些结果表明,用LGG和丁酸盐预处理可使Caco-2细胞感染空肠弯曲菌的初始阶段降至最低。

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