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Cell Host Microbe. 2014 Mar 12;15(3):374-81. doi: 10.1016/j.chom.2014.02.006.

Gut microbiota promote hematopoiesis to control bacterial infection.

Author information

1
Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA 91125, USA.
2
Regenerative Medicine Institute and Research Division of Immunology, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
3
Department of Oncological Sciences, Tisch Cancer Institute and Immunology Institute, Mount Sinai School of Medicine, New York, NY 10029, USA.
4
Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA 91125, USA. Electronic address: sarkis@caltech.edu.

Abstract

The commensal microbiota impacts specific immune cell populations and their functions at peripheral sites, such as gut mucosal tissues. However, it remains unknown whether gut microbiota control immunity through regulation of hematopoiesis at primary immune sites. We reveal that germ-free mice display reduced proportions and differentiation potential of specific myeloid cell progenitors of both yolk sac and bone marrow origin. Homeostatic innate immune defects may lead to impaired early responses to pathogens. Indeed, following systemic infection with Listeria monocytogenes, germ-free and oral-antibiotic-treated mice display increased pathogen burden and acute death. Recolonization of germ-free mice with a complex microbiota restores defects in myelopoiesis and resistance to Listeria. These findings reveal that gut bacteria direct innate immune cell development via promoting hematopoiesis, contributing to our appreciation of the deep evolutionary connection between mammals and their microbiota.

PMID:
24629343
PMCID:
PMC4144825
DOI:
10.1016/j.chom.2014.02.006
[Indexed for MEDLINE]
Free PMC Article
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