RT Journal Article SR Electronic T1 Toxoplasma gondii chronic infection decreases visceral nociception through peripheral opioid receptor signaling JF bioRxiv FD Cold Spring Harbor Laboratory SP 2024.09.13.612908 DO 10.1101/2024.09.13.612908 A1 Audibert, Alexis A1 Mas-Orea, Xavier A1 Rey, Léa A1 Belloy, Marcy A1 Bassot, Emilie A1 Marodon, Gilles A1 Masson, Frederick A1 Cenac, Nicolas A1 Dietrich, Gilles A1 Bonnart, Chrystelle A1 Blanchard, Nicolas YR 2024 UL http://biorxiv.org/content/early/2024/09/19/2024.09.13.612908.abstract AB 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 humansCompeting Interest StatementThe authors have declared no competing interest.