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...
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| Veröffentlicht in: | PLoS pathogens Jg. 21; H. 4 |
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Cold Spring Harbor Laboratory
19.09.2024
Public Library of Science |
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| 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.
Latent toxoplasmosis decreases gut nociception in the mouse, suggesting a negative association with abdominal pain in humans |
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| AbstractList | 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. Teaser Latent toxoplasmosis decreases gut nociception in the mouse, suggesting a negative association with abdominal pain in humans 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. Latent toxoplasmosis decreases gut nociception in the mouse, suggesting a negative association with abdominal pain in humans |
| Author | Blanchard, Nicolas Audibert, Alexis Rey, Léa Dietrich, Gilles Belloy, Marcy Cenac, Nicolas Masson, Frederick Mas-Orea, Xavier Bassot, Emilie Marodon, Gilles Bonnart, Chrystelle |
| Author_xml | – sequence: 1 givenname: Alexis surname: Audibert fullname: Audibert, Alexis organization: University Toulouse III - Paul Sabatier (UPS) – sequence: 2 givenname: Xavier surname: Mas-Orea fullname: Mas-Orea, Xavier organization: University Toulouse III - Paul Sabatier (UPS) – sequence: 3 givenname: Léa surname: Rey fullname: Rey, Léa organization: University Toulouse III - Paul Sabatier (UPS) – sequence: 4 givenname: Marcy surname: Belloy fullname: Belloy, Marcy organization: University Toulouse III – sequence: 5 givenname: Emilie surname: Bassot fullname: Bassot, Emilie organization: University Toulouse III – sequence: 6 givenname: Gilles surname: Marodon fullname: Marodon, Gilles organization: Sorbonne University – sequence: 7 givenname: Frederick surname: Masson fullname: Masson, Frederick organization: University Toulouse III – sequence: 8 givenname: Nicolas surname: Cenac fullname: Cenac, Nicolas organization: University Toulouse III - Paul Sabatier (UPS) – sequence: 9 givenname: Gilles surname: Dietrich fullname: Dietrich, Gilles organization: University Toulouse III - Paul Sabatier (UPS) – sequence: 10 givenname: Chrystelle surname: Bonnart fullname: Bonnart, Chrystelle email: nicolas.blanchard@inserm.fr organization: University Toulouse III - Paul Sabatier (UPS) – sequence: 11 givenname: Nicolas orcidid: 0000-0002-4924-2161 surname: Blanchard fullname: Blanchard, Nicolas email: nicolas.blanchard@inserm.fr organization: University Toulouse III |
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| Title | Toxoplasma gondii chronic infection decreases visceral nociception through peripheral opioid receptor signaling |
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