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Infection and Immunity, January 2009, p. 85-97, Vol. 77, No. 1
0019-9567/09/$08.00+0 doi:10.1128/IAI.01022-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Department of Developmental and Molecular Biology,1 Department of Obstetrics and Gynecology and Women's Health,2 Center for the Study of Reproductive Biology and Women's Health, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 104613
Received 16 August 2008/ Returned for modification 22 September 2008/ Accepted 7 October 2008
The association between extreme-prematurity births and intrauterine infection emphasizes the importance of understanding the host immune responses against uterine-invading microbes during early pregnancy to the prevention of preterm births. Listeria monocytogenes, a clinically relevant intracellular bacterium, has a predilection for replication at the maternofetal interface during pregnancy. Here, using mice carrying the recessive null osteopetrotic mutation in the colony-stimulating factor-1 (CSF-1) gene, we show that CSF-1-dependent macrophage functions are required for the maternal decidua immune responses against L. monocytogenes infections during early gestation in mice. In the absence of CSF-1, pregnant mice were more susceptible to uterine infection by L. monocytogenes; their inability to control the expansion of colonized bacteria in the pregnant uterus led to decidual cell death, tissue disintegration, and resorption of the developing embryo. However, CSF-1-deficient mice were able to produce significant levels of both Th1 cytokines and neutrophil chemoattractants and to recruit neutrophils to the decidual tissue in response to Listeria infection. Depletion of macrophages in hormonally induced pseudopregnant mice resulted in higher uterine bacterial levels after L. monocytogenes infection. These data suggest that the anti-Listeria responses in the maternal decidual tissue are dependent on CSF-1-regulated macrophages.
Published ahead of print on 13 October 2008.
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