Toxoplasma gondii chronic infection decreases visceral nociception through peripheral opioid receptor signaling

By eliciting immune activation in the digestive tract, intestinal pathogens may perturb gut homeostasis. Some gastrointestinal infections can indeed increase the risk of developing post-infectious irritable bowel syndrome (PI-IBS). Intriguingly, the prevalent foodborne parasite Toxoplasma gondii has not been linked to the development of PI-IBS and the impact of this infection on colon homeostasis remains ill-defined. We show in a mouse model that latent T. gondii decreases visceral nociceptive responses in an opioid signaling-dependent manner. Despite the accumulation of Th1 and cytotoxic T cells in the colon of latently infected mice, the selective invalidation of enkephalin gene in T cells ruled out the involvement of T cell-derived enkephalins in hypoalgesia. These findings provide clues about how this widespread infection durably shapes the gut immune landscape and modifies intestinal physiological parameters. They suggest that in contrast to other gut microbes, T. gondii infection could be negatively associated with abdominal pain.

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Publication Details

Journal
PLoS Pathogens
Published
2025-04-29
DOI
https://doi.org/10.1371/journal.ppat.1013106
Primary Topic
Toxoplasma gondii Research Studies
Type
article
Field-Weighted Citation Impact
0.00

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article

Toxoplasma gondii chronic infection decreases visceral nociception through peripheral opioid receptor signaling

Frédérick Masson, Nicolas Cénac, Chrystelle Bonnart, Matteo Sérino et al.
PLoS Pathogens
Toxoplasma gondii Research Studies
article

Toxoplasma gondii chronic infection decreases visceral nociception through peripheral opioid receptor signaling

Frédérick Masson, Nicolas Cénac, Chrystelle Bonnart, Matteo Sérino, Gilles Dietrich, Marcy Belloy, Emilie Bassot, Gilles Marodon, Louise Battut, Léa Rey, Nicolas Blanchard, Xavier Mas‐Orea, Alexis Audibert
article en

Abstract

By eliciting immune activation in the digestive tract, intestinal pathogens may perturb gut homeostasis. Some gastrointestinal infections can indeed increase the risk of developing post-infectious irritable bowel syndrome (PI-IBS). Intriguingly, the prevalent foodborne parasite Toxoplasma gondii has not been linked to the development of PI-IBS and the impact of this infection on colon homeostasis remains ill-defined. We show in a mouse model that latent T. gondii decreases visceral nociceptive responses in an opioid signaling-dependent manner. Despite the accumulation of Th1 and cytotoxic T cells in the colon of latently infected mice, the selective invalidation of enkephalin gene in T cells ruled out the involvement of T cell-derived enkephalins in hypoalgesia. These findings provide clues about how this widespread infection durably shapes the gut immune landscape and modifies intestinal physiological parameters. They suggest that in contrast to other gut microbes, T. gondii infection could be negatively associated with abdominal pain.

PLoS PathogensVol. 21(4)
Centre National de la Recherche Scientifique (FR), Inserm (FR), École Nationale Vétérinaire de Toulouse (FR), Université Fédérale de Toulouse Midi-Pyrénées (FR), Sorbonne Université (FR), Institut National de Recherche pour l'Agriculture, l'Alimentation et l'Environnement (FR), Toulouse Mathematics Institute (FR), Institut de Recherche en Santé Digestive (FR), Centre d'Immunologie et des Maladies Infectieuses (FR)
Agence Nationale de la Recherche, Fondation pour la Recherche Médicale
Zero hunger
Openalex Percentile: Top 91%
Toxoplasma gondii Research Studies
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