Innate immune function of the human decidual cell at the maternal–fetal interface

Canavan, Timothy P.; Simhan, Hyagriv N.

doi:10.1016/j.jri.2006.10.004

Cited by 48 publications

(45 citation statements)

References 25 publications

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“…Recent reports from studies of human tissue have suggested that functional Toll-like receptors are expressed in the decidua (10,33) and that antimicrobial peptides are produced in the first-trimester decidua (32) and the choriodecidua (9), which provided a basis for the decidual tissue to detect microbes and play a role in the maternal defense against bacterial infection during early pregnancy. It is interesting to observe by light microscopy that Listeria seems to be restricted to endocytic/ lysosomal vesicles in decidual cells (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…Recent reports from studies with human tissue have suggested the expression of functional Toll-like receptors in the decidua (10,33) and the production of antimicrobial peptides in the first-trimester decidua (32) and the choriodecidua (9), suggesting that decidual tissue might possibly play a role in the maternal defense against bacterial infection during early pregnancy. To further test this possibility, we infected pregnant mice that were homozygous or heterozygous for the mutation in the CSF-1 gene with intravenous (i.v.)…”

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confidence: 99%

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Colony-Stimulating Factor-1-Dependent Macrophage Functions Regulate the Maternal Decidua Immune Responses againstListeria monocytogenesInfections during Early Gestation in Mice

Qiu¹,

Zhu

Pollard

2009

Infect Immun

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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.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Colony-Stimulating Factor-1-Dependent Macrophage Functions Regulate the Maternal Decidua Immune Responses againstListeria monocytogenesInfections during Early Gestation in Mice

Qiu¹,

Zhu

Pollard

2009

Infect Immun

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“…Transcripts for TLRs 1-6 have been detected in term decidual cells but only TLR1, TLR2, TLR4 and TLR6 where shown to be functional via production of IL-8 in response to stimulation with LPS or PGN (Canavan and Simhan 2007). Immunohistochemical studies have demonstrated the expression of NOD1 and NOD2 in first trimester decidualised stroma (King, Horne et al 2009).…”

Section: Deciduamentioning

confidence: 99%

Cytokines and the Innate Immune Response at the Materno-Fetal Interface

Bryant¹,

Thornton²

2012

Recent Advances in Research on the Human Placenta

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“…TLR3 and TLR4 were mostly localized to the uterine glandular and luminal epithelium. In addition, TLR4 was specifically present on endometrial dendritic cells and inflammatory cells such as monocytes and macrophages [21]. To a lesser degree, TLRs 1, 2, 5, and 6 were present in the epithelia of different regions of the female reproductive tract.…”

Section: Pathogenesis Of Preterm Labormentioning

confidence: 99%

“…Transcripts for TLRs 1–10 have been detected in the human placenta [20]. Functional studies have shown specific expression of TLRs 2, 3 and 4 on trophoblasts, TLRs 2 and 4 expression on amniotic cells, and TLRs 1, 2, 4 and 6 expression on decidual cells [20,21]. …”

Section: Pathogenesis Of Preterm Labormentioning

confidence: 99%

Anticytokine Therapy in Preterm Labor: Current Knowledge and Future Perspectives

Sado

Kitanaka²,

Naruse³

et al. 2010

Gynecol Obstet Invest

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Aims: Up to 10% of pregnant women have preterm birth that might be refractory to current therapy. Infections and asphyxia related to preterm birth are the causes of death in the majority of neonates and therefore represent an urgent clinical need. Methods: The present article reviews the English language literature for preclinical and clinical trials and promising molecular targets on preterm labor. Results: Preterm birth is a complex heterogeneous condition. There is no current treatment for the fetal membranes once they have ruptured; therefore, essentially any treatment has to be preventative to quiesce preterm labor and prevent any spread of infection to the fetus. Modulating the pro-inflammatory process-mediated cytokine network may present a new paradigm for preterm labor treatment. There are many reports on the role of β-adrenergic agonists (betamimetics), magnesium sulfate, progesterone, oxytocin antagonist, calcium channel blocker or the Kunitz inhibitor bikunin in the treatment of preterm labor. In the present review, we have focused on the preclinical and clinical anticytokine therapy for preterm labor. The preclinical and clinical trials with bikunin reducing preterm labor exacerbations have raised the importance of usefulness and safety considerations related to this novel therapy. Conclusion: Anticytokine therapy is ready for the clinic.

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Innate immune function of the human decidual cell at the maternal–fetal interface

Cited by 48 publications

References 25 publications

Colony-Stimulating Factor-1-Dependent Macrophage Functions Regulate the Maternal Decidua Immune Responses againstListeria monocytogenesInfections during Early Gestation in Mice

Colony-Stimulating Factor-1-Dependent Macrophage Functions Regulate the Maternal Decidua Immune Responses againstListeria monocytogenesInfections during Early Gestation in Mice

Cytokines and the Innate Immune Response at the Materno-Fetal Interface

Anticytokine Therapy in Preterm Labor: Current Knowledge and Future Perspectives

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