Clostridium butyricum relieve the visceral hypersensitivity in mice induced by Citrobacter rodentium infection with chronic stress.
Clostridium butyricum relieve the visceral hypersensitivity in mice induced by Citrobacter rodentium infection with chronic stress.
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丁酸梭菌缓解啮齿类柠檬酸杆菌感染慢性应激小鼠内脏过敏
作者：
Wang T;Li L;Li S;Zhao H;Qu J;Xia Y;Li Y
背景内脏过敏是感染后肠易激综合征（PI-IBS）患者的常见症状，肠道菌群的改变是其重要的致病因素。丁酸菌）是一种益生菌，据报道其作为活性成分用于治疗IBS，尤其是伴有腹泻的IBS。啮齿类柠檬酸杆菌（Citrobacter rodentium，C. rodentium）是一种肠道致病菌，其可在小鼠中产生自限性结肠炎，其已被用于产生PI-IBS样小鼠模型。无论C.丁酸可能影响PI-IBS的内脏高敏感性和肠道微生物群仍然是未知的。本研究旨在探讨C.丁酸或抗生素可能影响内脏高敏感性的病因。方法C57 BL/6雄性小鼠灌胃C.引发感染性结肠炎梭3天后用酪酸和抗生素复合物干预感染小鼠。采用为期9天的慢性避水应激（WAS）过程来诱导内脏高敏感性。以腹部退缩反射（AWR）评分反映内脏高敏感性。在感染后的第7、14和30天，收集小鼠粪便并进行高通量测序以分析其肠道微生物群。综合结果，C.啮齿动物感染加慢性应激（WAS）可诱导小鼠内脏高敏感性。对C. butyricum后C.啮齿动物感染可减轻小鼠内脏高敏感性，而抗生素治疗组无明显差异。C.肠道菌群多样性感染鼠与未感染鼠的微生物区系结构相似，但两者的微生物区系结构不同。感染后第7、14、30天，抗生素治疗组的Shannon指数和Chao指数均显著低于其他组，而C.酪酸可使上述指标维持在正常范围内。感染后第14天，C.丁酸治疗。WAS后，对照组的Shannon指数和Chao指数下降，微生物群结构发生变化。梭酪酸处理可以防止WAS诱导的肠道微生物群的这些变化。结论C.丁酸钠能减轻C.啮齿类感染加上慢性压力它还可以重塑由感染和慢性压力引起的微生物群变化。这可能是一种比抗生素更有效的治疗PI-IBS的策略。
Background Visceral hypersensitivity is a common symptom in patients with post-infectious irritable bowel syndrome (PI-IBS), and change of the microbiota is a vital etiological factor of it. Clostridium butyricum (C. butyricum) is one of the probiotics which is reported as the active components in the treatment of IBS, especially IBS with diarrhea. Citrobacter rodentium (C. rodentium) is an enteropathogenic bacteria which can produce self-limiting colitis in mice, which have been used to produce a PI-IBS-like mice model. Whether C. butyricum could influence the visceral hypersensitivity and gut microbiota of PI-IBS is still unknown. Our study aimed to examine whether the intervention of C. butyricum or antibiotics could affect the etiology of visceral hypersensitivity. Methods C57BL/6 male mice were gavaged with the C. rodentium to induce a infective colitis. The C. butyricum and antibiotic compound were used to intervene the infected mice 3 days later. A 9-day chronic water avoidance stress (WAS) process was implemented to help induce the visceral hypersensitivity. The abdominal withdrawal reflex (AWR) score was assayed to indicate the visceral hypersensitivity of different groups. On the 7th, 14th, and 30th days after infection, mice feces were collected and high-throughput sequencing was carried out to analyze their gut microbiota. Results Combined, the C. rodentium infection plus chronic stress (WAS) could induce the visceral hypersensitivity in mice. Treatment of the C. butyricum after C. rodentium infection could relieve visceral hypersensitivity of mice, while no difference was observed in the antibiotic treatment group. The gut microbiota diversity of C. rodentium infected mice was similar to the uninfected mice, while there were different microbial communities structure between them. The Shannon and Chao indexes significantly decreased in the antibiotic treatment group compared to other groups at 7th, 14th, and 30th days post-infection, while treatment of C. butyricum could maintain the indexes within normal range. At day 14 after infection, the structure of microbiota headed towards normality after the C. butyricum treatment. After the WAS, the Shannon and Chao indexes of the control group decreased and the structure of microbiota changed. The C. butyricum treatment could prevent these changes of the gut microbiota induced by WAS. Conclusion C. butyricum could relieve the visceral hypersensitivity in mice induced by C. rodentium infection plus chronic stress. It could also remodel the microbiota change caused by the infection and chronic stress. It may be a more effective treatment strategy for PI-IBS than antibiotics.
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DOI：
10.1073/pnas.1812901116
发表时间：
2019-03-19
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