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共生菌 P. UF1 对新生儿肠道免疫的调节作用

Neonatal intestinal immune regulation by the commensal bacterium, P. UF1.

机构信息

Department of Infectious Diseases & Immunology, University of Florida, Gainesville, FL, USA.

Division of Gastroenterology, Hepatology & Nutrition, Department of Medicine, University of Florida, Gainesville, FL, USA.

出版信息

Mucosal Immunol. 2019 Mar;12(2):434-444. doi: 10.1038/s41385-018-0125-1. Epub 2019 Jan 15.

DOI:10.1038/s41385-018-0125-1
PMID:30647410
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6375783/
Abstract

Newborns are highly susceptible to pathogenic infections with significant worldwide morbidity possibly due to an immature immune system. Recently, we reported that Propionibacterium strain, P. UF1, isolated from the gut microbiota of preterm infants, induced the differentiation of bacteria-specific Th17 cells. Here, we demonstrate that P. UF1 significantly increased the number of protective Th17 cells and maintained IL-10 regulatory T cells (Tregs) in newborn mice. In addition, P. UF1 protected mice from intestinal Listeria monocytogenes (L. m) infection. P. UF1 also functionally sustained the gut microbiota and induced critical B vitamin metabolites implicated in the regulation of T cell immunity during L. m intestinal infection. Transcriptomic analysis of P. UF1-induced Th17 cells revealed genes involved in the differentiation and regulation of these cells. These results illustrate the potency of P. UF1 in the enhancement of neonatal host defense against intestinal pathogen infection.

摘要

新生儿极易受到病原感染,具有很高的发病率,这可能是由于其免疫系统不成熟。最近,我们报道了从早产儿肠道微生物群中分离出的丙酸杆菌菌株 P. UF1 可诱导细菌特异性 Th17 细胞分化。在这里,我们证明 P. UF1 可显著增加保护性 Th17 细胞的数量,并维持新生小鼠中的 IL-10 调节性 T 细胞(Tregs)。此外,P. UF1 可保护小鼠免受肠道李斯特菌(L. m)感染。P. UF1 还可维持肠道微生物群的功能,并诱导在 L. m 肠道感染期间参与调节 T 细胞免疫的关键 B 族维生素代谢物。对 P. UF1 诱导的 Th17 细胞的转录组分析显示了涉及这些细胞分化和调节的基因。这些结果说明了 P. UF1 在增强新生儿宿主防御肠道病原体感染方面的强大作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ffb/6375783/01598d25ef7d/nihms-1516537-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ffb/6375783/a7a16c5225f2/nihms-1516537-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ffb/6375783/9ad583fd22d2/nihms-1516537-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ffb/6375783/f92d97d9d14a/nihms-1516537-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ffb/6375783/714d056925a3/nihms-1516537-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ffb/6375783/01598d25ef7d/nihms-1516537-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ffb/6375783/a7a16c5225f2/nihms-1516537-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ffb/6375783/9ad583fd22d2/nihms-1516537-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ffb/6375783/f92d97d9d14a/nihms-1516537-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ffb/6375783/714d056925a3/nihms-1516537-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ffb/6375783/01598d25ef7d/nihms-1516537-f0005.jpg

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建立友谊:新生儿免疫系统主动选择共生体和排斥病原体。
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Murine in utero exposure to simulated complex urban air pollution disturbs offspring gut maturation and microbiota during intestinal suckling-to-weaning transition in a sex-dependent manner.孕期暴露于模拟的复杂城市空气污染会以性别依赖的方式干扰后代在肠道哺乳到断奶过渡期的肠道成熟和微生物群。
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Early Postnatal Comprehensive Biomarkers Cannot Identify Extremely Preterm Infants at Risk of Developing Necrotizing Enterocolitis.出生后早期综合生物标志物无法识别有发生坏死性小肠结肠炎风险的极早产儿。
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