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Toxoplasma gondii dictates placental trophoblast lineage specification through induction of decidual signaling cues [CV_bulkRNA-seq]

ABSTRACT: Pregnancy is a critical point of vulnerability to infection and other insults that could compromise proper fetal development. The placenta acts as a protective barrier to most infectious agents, though a few are capable of bypassing its defenses. Little is known about how exposure to these select pathogens impacts ongoing placental development. We demonstrate thatToxoplasma entirely misdirects the developmental program of trophoblast stem cells. Infection of progenitor cytotrophoblasts prevents fusion and differentiation to infection-resistant syncytiotrophoblasts. Rather, Toxoplasma elicits a transcriptional profile that polarizes cytotrophoblasts to the infection-permissive extravillous trophoblast fate across three orthogonal models: trophoblast stem cells, trophoblast organoids, and chorionic villi. Manipulation of cell fate by the parasite is most dramatic in organoids, where we see robust outgrowth of HLA-G(+) extravillous trophoblasts. These data show thatToxoplasmaantagonizes differentiation of an infection-resistant lineage by inducing formation of an infection-permissive lineage, therefore potentiating its own transmission to the fetus.

ORGANISM(S): Homo sapiens

PROVIDER: GSE276116 | GEO | 2026/09/01

REPOSITORIES: GEO

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Toxoplasma gondii dictates placental trophoblast lineage specification through induction of decidual signaling cues [TO_bulkRNA-seq]

Project description:Pregnancy is a critical point of vulnerability to infection and other insults that could compromise proper fetal development. The placenta acts as a protective barrier to most infectious agents, though a few are capable of bypassing its defenses. Little is known about how exposure to these select pathogens impacts ongoing placental development. We demonstrate thatToxoplasma entirely misdirects the developmental program of trophoblast stem cells. Infection of progenitor cytotrophoblasts prevents fusion and differentiation to infection-resistant syncytiotrophoblasts. Rather, Toxoplasma elicits a transcriptional profile that polarizes cytotrophoblasts to the infection-permissive extravillous trophoblast fate across three orthogonal models: trophoblast stem cells, trophoblast organoids, and chorionic villi. Manipulation of cell fate by the parasite is most dramatic in organoids, where we see robust outgrowth of HLA-G(+) extravillous trophoblasts. These data show thatToxoplasmaantagonizes differentiation of an infection-resistant lineage by inducing formation of an infection-permissive lineage, therefore potentiating its own transmission to the fetus.

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