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热灭活嗜热链球菌菌株7对炎症反应的调节作用:对TLR3诱导的肠道损伤动物模型的研究

Modulatory Effects of Heat-Inactivated Streptococcus Thermophilus Strain 7 on the Inflammatory Response: A Study on an Animal Model with TLR3-Induced Intestinal Injury.

作者信息

Lee Gilbert Aaron, Chang Yu-Wei, Lin Wan-Li, Yang Yu-Chen S H, Chen Wei-Jen, Huang Fu-Huan, Liu Yun-Ru

机构信息

Department of Medical Research, Taipei Medical University Hospital, Taipei City 110, Taiwan.

Department of Microbiology and Immunology, School of Medicine, College of Medicine, Taipei Medical University, Taipei City 110, Taiwan.

出版信息

Microorganisms. 2023 Jan 20;11(2):278. doi: 10.3390/microorganisms11020278.

Abstract

Rotavirus infections result in severe gastroenteritis with a detrimental inflammatory response in the intestine. Because probiotics have an anti-inflammatory effect and can modulate the gut microbiota profile, they can be used as a biotherapy for inflammatory intestinal diseases. In this study, we isolated strain 7 (ST7) from cow milk and examined the effect of heat-inactivated ST7 on the intestinal histopathological score, inflammatory cytokine levels, T-cell activation and effector function, and microbiome profile in a mouse model with intestinal injury induced by polyinosinic-polycytidylic acid (poly I:C), a Toll-like receptor 3 agonist. The results indicated that ST7 treatment prevented weight loss and intestinal injury and prevented the upregulation of serum interleukin-6 (IL-6), tumor necrosis factor-α, and IL-15 levels in intestinal epithelial cells; prevented the upregulation of inflammation-associated Gammaproteobacteria and ; and increased the levels of Firmicutes in fecal microbiota after poly I:C stimulation. ST7 treatment also increased the serum interferon-γ (IFN-γ) level and promoted the expression of IFN-γ in both CD8 and CD4 T cells. In summary, ST7 prevented the inflammatory response, promoted the T-cell effector function, and modulated the microbiota profile of mice with poly I:C-induced small intestine injury.

摘要

轮状病毒感染会导致严重的肠胃炎,并在肠道引发有害的炎症反应。由于益生菌具有抗炎作用且能调节肠道微生物群谱,因此可作为炎症性肠病的生物疗法。在本研究中,我们从牛奶中分离出菌株7(ST7),并在由Toll样受体3激动剂聚肌苷酸-聚胞苷酸(poly I:C)诱导肠道损伤的小鼠模型中,检测了热灭活ST7对肠道组织病理学评分、炎性细胞因子水平、T细胞活化及效应功能以及微生物群谱的影响。结果表明,ST7处理可防止体重减轻和肠道损伤,并防止肠道上皮细胞中血清白细胞介素-6(IL-6)、肿瘤坏死因子-α和IL-15水平上调;防止炎症相关γ-变形菌的上调以及 ;并在poly I:C刺激后增加粪便微生物群中厚壁菌门的水平。ST7处理还提高了血清干扰素-γ(IFN-γ)水平,并促进了CD8和CD4 T细胞中IFN-γ的表达。总之,ST7可预防炎症反应,促进T细胞效应功能,并调节poly I:C诱导的小肠损伤小鼠的微生物群谱。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bae/9959611/fe2232b51ab8/microorganisms-11-00278-g001.jpg

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