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Commensal Propionibacterium strain UF1 mitigates intestinal inflammation via Th17 cell regulation.

Authors
  • Colliou, Natacha1, 2
  • Ge, Yong1, 2
  • Sahay, Bikash1
  • Gong, Minghao1, 2
  • Zadeh, Mojgan1, 2
  • Owen, Jennifer L3
  • Neu, Josef4
  • Farmerie, William G5
  • Alonzo, Francis 3rd6
  • Liu, Ken7
  • Jones, Dean P7
  • Li, Shuzhao7
  • Mohamadzadeh, Mansour1, 2
  • 1 Department of Infectious Diseases and Immunology.
  • 2 Division of Gastroenterology, Hepatology & Nutrition, Department of Medicine.
  • 3 Department of Physiological Sciences.
  • 4 Division of Neonatology, Department of Pediatrics, and.
  • 5 Interdisciplinary Center for Biotechnology Research, University of Florida, Gainesville, Florida, USA.
  • 6 Department of Microbiology and Immunology, Loyola University Chicago, Maywood, Illinois, USA.
  • 7 Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia, USA. , (Georgia)
Type
Published Article
Journal
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Publication Date
Nov 01, 2017
Volume
127
Issue
11
Pages
3970–3986
Identifiers
DOI: 10.1172/JCI95376
PMID: 28945202
Source
Medline
License
Unknown

Abstract

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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