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益生菌诱导的肠道微生物群变化可抑制弓形虫感染。

Probiotic-induced changes in intestinal microbiome inhibits Toxoplasma gondii infection.

作者信息

Lee Hak-Jae, Ham Do-Won, Seo Seung-Hwan, Cha Guang-Ho, Shin Eun-Hee

机构信息

Department of Tropical Medicine and Parasitology, Seoul National University College of Medicine, Seoul 03080, Korea.

Institute of Endemic Diseases, Medical Research Center, Seoul National University, Seoul 03080, Korea.

出版信息

Parasites Hosts Dis. 2024 Nov;62(4):408-423. doi: 10.3347/PHD.24068. Epub 2024 Nov 22.

DOI:10.3347/PHD.24068
PMID:39622653
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11614487/
Abstract

Toxoplasma gondii primarily invades the central nervous system, causing latent infections. Cysts persist in the host for life and there is currently no effective treatment. T. gondii infects human hosts through contaminated meat, invading the intestinal tissue and leading to changes in the number and composition of the gut microbiota. Since probiotic ingestion modulates intestinal microbiota changes, we hypothesized that intestinal microbiota dysbiosis caused by T. gondii infection would be restored following probiotic supplementation. To this end, we orally infected C57BL/6 mice with 10 T. gondii cysts and administered supplemental probiotics daily. We analyzed the levels of T. gondii B1 gene DNA, indicative of T. gondii infection, in brain tissue. We investigated alterations in the gut microbiota composition and functional pathways between the probiotic and non-probiotic treatment groups via next-generation sequencing analysis of each fecal sample. The infection level in the probiotic-treated group was significantly reduced after 4 weeks (p<0.05). Probiotic supplementation notably changed the gut microbiota after 2 weeks of infection, increasing the relative abundance of Intestinimonas massiliensis and Lawsonibacter asaccharolyticus. Probiotic supplements appear to modulate the gut microbiota, activating functional pathways involved in intestinal short-chain fatty acid production and strengthening the intestinal barrier, thereby impeding T. gondii infection and subsequent proliferation. Our findings provide valuable insights into T. gondii infection control and future study directions.

摘要

刚地弓形虫主要侵袭中枢神经系统,引发潜伏感染。包囊在宿主体内终身存在,目前尚无有效的治疗方法。刚地弓形虫通过受污染的肉类感染人类宿主,侵入肠道组织并导致肠道微生物群数量和组成发生变化。由于摄入益生菌可调节肠道微生物群的变化,我们推测,补充益生菌后,由刚地弓形虫感染引起的肠道微生物群失调将得到恢复。为此,我们给C57BL/6小鼠口服感染10个刚地弓形虫包囊,并每天给予补充益生菌。我们分析了脑组织中指示刚地弓形虫感染的刚地弓形虫B1基因DNA水平。通过对每个粪便样本进行二代测序分析,我们研究了益生菌治疗组和非益生菌治疗组之间肠道微生物群组成和功能途径的变化。4周后,益生菌治疗组的感染水平显著降低(p<0.05)。感染2周后,补充益生菌显著改变了肠道微生物群,增加了马赛肠单胞菌和非糖解劳森菌的相对丰度。益生菌补充剂似乎可以调节肠道微生物群,激活参与肠道短链脂肪酸产生的功能途径,并加强肠道屏障,从而阻碍刚地弓形虫的感染和后续增殖。我们的研究结果为刚地弓形虫感染控制和未来的研究方向提供了有价值的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce94/11614487/b41c77cc1753/phd-24068f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce94/11614487/b41c77cc1753/phd-24068f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce94/11614487/b41c77cc1753/phd-24068f5.jpg

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本文引用的文献

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