Tissue-specific transcriptomic responses to early Toxoplasma gondii infection in sheep during congenital toxoplasmosis
- 1Universidad Complutense de Madrid
Abstract
Toxoplasma gondii is a widespread zoonotic pathogen of major One Health concern, capable of causing congenital toxoplasmosis in both humans and sheep. Despite its impact, early host-parasite molecular interactions during acute infection in pregnant hosts remain largely unexplored. In this study, we characterized the transcriptomic responses of key tissues involved in early infection (the small intestine, mesenteric lymph nodes, and placenta) in pregnant ewes experimentally infected with T. gondii strain TgShSp1. RNA-seq analysis revealed pronounced, tissue-specific transcriptional changes at 6 days post-infection (dpi), particularly in the mesenteric lymph nodes, characterized by activation of interferon- and cytokine-mediated immune pathways. In contrast, transcriptional responses at 3 dpi were limited, consistent with a silent phase of parasite dissemination. Despite the absence of detectable parasite DNA, placentomes showed modest interferon-associated responses and upregulation of DNA repair and cellular stress pathways. These changes coincided with marked suppression of cell-cycle progression and extracellular matrix remodeling alongside inhibition of angiogenesis and hypoxia pathways. Altogether, early disruption of placental vascular function and tissue remodeling may contribute to fetal loss. In summary, these findings provide new insights into early host responses to T. gondii infection in a pregnant host and identify molecular mechanisms that may predispose to early fetal death during ovine congenital toxoplasmosis.
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BibTeX
@misc{coronado2026tissuespecific,
title = {{Tissue-specific transcriptomic responses to early Toxoplasma gondii infection in sheep during congenital toxoplasmosis}},
author = {M. Coronado and R. Sanchez-Sanchez and A. Reyes-Palomares and N. Velasco-Jimenez and M. Silva and J. Benavides and L. M. ORTEGA MORA and P. Horcajo},
howpublished = {bioRxiv},
year = {2026},
month = oct,
doi = {10.64898/2026.10.27.762155},
url = {https://www.biorxiv.org/content/10.64898/2026.10.27.762155v1},
note = {CC BY-NC-ND},
}
RIS
TY - UNPB
TI - Tissue-specific transcriptomic responses to early Toxoplasma gondii infection in sheep during congenital toxoplasmosis
AU - M. Coronado
AU - R. Sanchez-Sanchez
AU - A. Reyes-Palomares
AU - N. Velasco-Jimenez
AU - M. Silva
AU - J. Benavides
AU - L. M. ORTEGA MORA
AU - P. Horcajo
PY - 2026
DA - 2026/10/27
PB - bioRxiv
DO - 10.64898/2026.10.27.762155
UR - https://www.biorxiv.org/content/10.64898/2026.10.27.762155v1
AB - Toxoplasma gondii is a widespread zoonotic pathogen of major One Health concern, capable of causing congenital toxoplasmosis in both humans and sheep. Despite its impact, early host-parasite molecular interactions during acute infection in pregnant hosts remain largely unexplored. In this study, we characterized the transcriptomic responses of key tissues involved in early infection (the small intestine, mesenteric lymph nodes, and placenta) in pregnant ewes experimentally infected with T. gondii strain TgShSp1. RNA-seq analysis revealed pronounced, tissue-specific transcriptional changes at 6 days post-infection (dpi), particularly in the mesenteric lymph nodes, characterized by activation of interferon- and cytokine-mediated immune pathways. In contrast, transcriptional responses at 3 dpi were limited, consistent with a silent phase of parasite dissemination. Despite the absence of detectable parasite DNA, placentomes showed modest interferon-associated responses and upregulation of DNA repair and cellular stress pathways. These changes coincided with marked suppression of cell-cycle progression and extracellular matrix remodeling alongside inhibition of angiogenesis and hypoxia pathways. Altogether, early disruption of placental vascular function and tissue remodeling may contribute to fetal loss. In summary, these findings provide new insights into early host responses to T. gondii infection in a pregnant host and identify molecular mechanisms that may predispose to early fetal death during ovine congenital toxoplasmosis.
ER -