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

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.

SUBMITTER: Ge Y

PROVIDER: S-EPMC6375783 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature

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

Ge Yong Y Gong Minghao M Colliou Natacha N Zadeh Mojgan M Li Jing J Jones Dean P DP Li Shuzhao S Mohamadzadeh Mansour M

Mucosal immunology 20190115 2

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<sup>+</sup> regulatory T cells (Tregs) in newborn mice. In addition, P. UF ...[more]

PMID: 30647410

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Project description:Neonatal immune challenge by administration of lipopolysaccharide (LPS) produces enduring alterations in the development and activity of neuroendocrine, immune and other physiological systems. We have recently reported that neonatal exposure to an immune challenge by administration of LPS results in altered reproductive development in the female Wistar rat. Specifically, LPS-treated animals exhibited diminished ovarian reserve and altered reproductive lifespan. In the current study, we examined the cellular mechanisms that lead to the previously documented impaired ovulation and reduced follicular pool. Rats were administered intraperitoneally either 0.05 mg/kg of LPS (Salmonella Enteritidis) or an equivalent volume of non-pyrogenic saline on postnatal days (PNDs) 3 and 5, and ovaries were obtained on PND 7. Microarray analysis revealed a significant upregulation in transcript expression (2-fold change; p < 0.05) for a substantial number of genes in the ovaries of LPS-treated animals, implicated in immune cell signaling, inflammatory responses, reproductive system development and disease. Several canonical pathways involved in immune recognition were affected by LPS treatment, such as nuclear factor-?B (NF-?B) activation and LPS-stimulated mitogen-activated protein kinase (MAPK) signaling. Quantitative Real-time PCR analysis supported the microarray results. Protein expression analysis of several components of the MAPK signaling pathway revealed a significant upregulation in the expression of Toll-like receptor 4 (TLR4) in the neonatal ovary of LPS-treated animals. These results indicate that neonatal immune challenge by administration of LPS has a direct effect on the ovary during the sensitive period of follicular formation. Given the pivotal role of inflammatory processes in the regulation of reproductive health, our findings suggest that early life immune activation via TLR signaling may have significant implications for the programming of ovarian development and fertility.

Dataset Information

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

Publications

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

Similar Datasets

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