{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ahrends T"],"funding":["Kenneth Rainin Foundation","Howard Hughes Medical Institute","NIDDK NIH HHS","National Institutes of Health"],"pagination":["5715-5727.e12"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8595755"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["184(23)"],"pubmed_abstract":["The enteric nervous system (ENS) controls several intestinal functions including motility and nutrient handling, which can be disrupted by infection-induced neuropathies or neuronal cell death. We investigated possible tolerance mechanisms preventing neuronal loss and disruption in gut motility after pathogen exposure. We found that following enteric infections, muscularis macrophages (MMs) acquire a tissue-protective phenotype that prevents neuronal loss, dysmotility, and maintains energy balance during subsequent challenge with unrelated pathogens. Bacteria-induced neuroprotection relied on activation of gut-projecting sympathetic neurons and signaling via β<sub>2</sub>-adrenergic receptors (β2AR) on MMs. In contrast, helminth-mediated neuroprotection was dependent on T cells and systemi"],"journal":["Cell"],"pubmed_title":["Enteric pathogens induce tissue tolerance and prevent neuronal loss from subsequent infections."],"pmcid":["PMC8595755"],"funding_grant_id":["R01DK116646","R01 DK126407","R01 DK116646","R01 DK110352","R01DK126407"],"pubmed_authors":["Ahrends T","Aydin B","Mucida D","Marchildon F","Lira SA","Classon CH","Matheis F","Furtado GC"],"additional_accession":[]},"is_claimable":false,"name":"Enteric pathogens induce tissue tolerance and prevent neuronal loss from subsequent infections.","description":"The enteric nervous system (ENS) controls several intestinal functions including motility and nutrient handling, which can be disrupted by infection-induced neuropathies or neuronal cell death. We investigated possible tolerance mechanisms preventing neuronal loss and disruption in gut motility after pathogen exposure. We found that following enteric infections, muscularis macrophages (MMs) acquire a tissue-protective phenotype that prevents neuronal loss, dysmotility, and maintains energy balance during subsequent challenge with unrelated pathogens. Bacteria-induced neuroprotection relied on activation of gut-projecting sympathetic neurons and signaling via β<sub>2</sub>-adrenergic receptors (β2AR) on MMs. In contrast, helminth-mediated neuroprotection was dependent on T cells and systemi","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Nov","modification":"2025-04-05T12:31:59.741Z","creation":"2025-04-05T12:31:59.741Z"},"accession":"S-EPMC8595755","cross_references":{"pubmed":["34717799"],"doi":["10.1016/j.cell.2021.10.004"]}}