ArticlePlacenta2013
IL-10 produced by trophoblast cells inhibits phagosome maturation leading to profound intracellular proliferation of Salmonella enterica Typhimurium.
Article in Placenta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Progesterone promotes maternal-fetal tolerance by reducing human maternal T-cell polyfunctionality and inducing a specific cytokine profile.European journal of immunology · 2015Trial
- tRF-His-GTG-1 promotes Salmonella survival through modulation of lipid metabolism and immune signaling.Cell communication and signaling : CCS · 2025Article
- Macrophages downregulate NEDD9 to counteract S. Typhimurium- mediated FAK-AKT activation and lysosome inhibition.Cell death & disease · 2025Article
- Analysis of the capacity of Salmonella enterica Typhimurium to infect the human Placenta.Placenta · 2019Article
- IL-27 amplifies cytokine responses to Gram-negative bacterial products and Salmonella typhimurium infection.Scientific reports · 2018Article
- Prostaglandins DJournal of lipid research · 2018Article
- Novel mechanism of miRNA-365-regulated trophoblast apoptosis in recurrent miscarriage.Journal of cellular and molecular medicine · 2017Article
- Rab11 family expression in the human placenta: Localization at the maternal-fetal interface.PloS one · 2017Article
- Interleukin-10 Production by T and B Cells Is a Key Factor to Promote SystemicFrontiers in immunology · 2017Article
- Distinct innate responses are induced by attenuated Salmonella enterica serovar Typhimurium mutants.Cellular immunology · 2016Article
- Malaria parasite infection compromises control of concurrent systemic non-typhoidal Salmonella infection via IL-10-mediated alteration of myeloid cell function.PLoS pathogens · 2014Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
introductionSalmonella enterica Typhimurium (ST) is a phagosomal pathogen that can infect placental trophoblast cells leading to abortion and severe maternal illness. It is unclear how the trophoblast cells promote profound bacterial proliferation.
methodsThe mechanism of internalization, intracellular growth and phagosomal biogenesis in ST-infected human epithelial (HeLa), macrophage (THP-1) and trophoblast-derived cell lines (JEG-3, BeWo and HTR-8) was studied. Specific inhibitors were used to block bacterial internalization. Phagosomal maturation was determined by confocal microscopy, Western-blotting and release of lysosomal β-galactosidase by infected cells. Bacterial colony forming units were determined by plating infected cell lysates on agar plates.
resultsST proliferated minimally in macrophages but replicated profoundly within trophoblast cells. The ST-ΔinvA (a mutant of Salmonella pathogenicity island-1 gene effector proteins) was unable to infect epithelial cells, but was internalized by scavenger receptors on trophoblasts and macrophages. However, ST was contrastingly localized in early (Rab5⁺) or late (LAMP1⁺) phagosomes within trophoblast cells and macrophages respectively. Furthermore trophoblast cells (unlike macrophages) did not exhibit phagoso-lysosomal fusion. ST-infected macrophages produced IL-6 whereas trophoblast cells produced IL-10. Neutralizing IL-10 in JEG-3 cells accelerated phagolysomal fusion and reduced proliferation of ST. Placental bacterial burden was curtailed in vivo in anti-IL-10 antibody treated and IL-10-deficient mice. DISCUSSION: Macrophages phagocytose but curtail intracellular replication of ST in late phagosomes. In contrast, phagocytosis by trophoblast cells results in an inappropriate cytokine response and proliferation of ST in early phagosomes.
conclusionIL-10 production by trophoblast cells that delays phagosomal maturation may facilitate proliferation of pathogens in placental cells.
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