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Updated: Jun 29, 2026
Human Placental and Decidual Organ Cultures to Study Infections at the Maternal-fetal Interface
Published on: July 21, 2016
Colony-stimulating factor-1-dependent macrophage functions regulate the maternal decidua immune responses against
Xuan Qiu1, Liyin Zhu, Jeffrey W Pollard
1Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.
Abstract:
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.
Insights
Colony-stimulating factor-1 (CSF-1) regulates maternal immune cells called macrophages. These macrophages are crucial for controlling uterine Listeria monocytogenes infections during early pregnancy, preventing preterm birth complications.
Area of Science:
- Immunology
- Reproductive Biology
- Microbiology
Background:
- Intrauterine infections are linked to preterm births.
- Listeria monocytogenes is a bacterium that can infect the maternofetal interface during pregnancy.
Purpose of the Study:
- To investigate the role of colony-stimulating factor-1 (CSF-1) and its dependent macrophages in maternal immune responses against Listeria monocytogenes during early gestation.
- To understand the mechanisms underlying preterm birth prevention related to uterine infections.
Main Methods:
- Utilized mice with a mutation in the CSF-1 gene (CSF-1-deficient mice).
- Infected pregnant mice with Listeria monocytogenes.
- Depleted macrophages in pseudopregnant mice to assess their role.
Main Results:
- CSF-1-dependent macrophage functions are essential for controlling uterine Listeria monocytogenes infection in early pregnancy.
- CSF-1 deficiency led to increased susceptibility to uterine infection, bacterial expansion, decidual cell death, and embryo resorption.
- Despite CSF-1 deficiency, Th1 cytokine production and neutrophil recruitment to the decidua occurred.
- Macrophage depletion increased uterine bacterial load, confirming their anti-Listeria role.
Conclusions:
- Maternal decidual immune responses against Listeria monocytogenes are dependent on CSF-1-regulated macrophages.
- These findings highlight the critical role of CSF-1-mediated macrophage activity in preventing pregnancy complications arising from uterine infections.
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