Commensal Propionibacterium strain UF1 mitigates intestinal inflammation via Th17 cell regulation.
Department of Infectious Diseases and Immunology.
Division of Gastroenterology, Hepatology & Nutrition, Department of Medicine.
Department of Physiological Sciences.
Division of Neonatology, Department of Pediatrics, and.
Interdisciplinary Center for Biotechnology Research, University of Florida, Gainesville, Florida, USA.
Department of Microbiology and Immunology, Loyola University Chicago, Maywood, Illinois, USA.
Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, USA.
- Published Article
Journal of Clinical Investigation
American Society for Clinical Investigation
- Publication Date
Nov 01, 2017
Consumption of human breast milk (HBM) attenuates the incidence of necrotizing enterocolitis (NEC), which remains a leading and intractable cause of mortality in preterm infants. Here, we report that this diminution correlates with alterations in the gut microbiota, particularly enrichment of Propionibacterium species. Transfaunation of microbiota from HBM-fed preterm infants or a newly identified and cultured Propionibacterium strain, P. UF1, to germfree mice conferred protection against pathogen infection and correlated with profound increases in intestinal Th17 cells. The induction of Th17 cells was dependent on bacterial dihydrolipoamide acetyltransferase (DlaT), a major protein expressed on the P. UF1 surface layer (S-layer). Binding of P. UF1 to its cognate receptor, SIGNR1, on dendritic cells resulted in the regulation of intestinal phagocytes. Importantly, transfer of P. UF1 profoundly mitigated induced NEC-like injury in neonatal mice. Together, these results mechanistically elucidate the protective effects of HBM and P. UF1-induced immunoregulation, which safeguard against proinflammatory diseases, including NEC.
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This record was last updated on 06/09/2018 and may not reflect the most current and accurate biomedical/scientific data available from NLM.
The corresponding record at NLM can be accessed at https://www.ncbi.nlm.nih.gov/pubmed/28945202