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dc.contributor.authorLabed, Sid Ahmed
dc.contributor.authorWani, Khursheed A.
dc.contributor.authorJagadeesan, Sakthimala
dc.contributor.authorHakkim, Abdul
dc.contributor.authorNajibi, Mehran
dc.contributor.authorIrazoqui, Javier E
dc.date2022-08-11T08:09:18.000
dc.date.accessioned2022-08-23T16:26:12Z
dc.date.available2022-08-23T16:26:12Z
dc.date.issued2018-05-15
dc.date.submitted2020-03-13
dc.identifier.citation<p>Immunity. 2018 May 15;48(5):963-978.e3. doi: 10.1016/j.immuni.2018.04.017. <a href="https://doi.org/10.1016/j.immuni.2018.04.017">Link to article on publisher's site</a></p>
dc.identifier.issn1074-7613 (Linking)
dc.identifier.doi10.1016/j.immuni.2018.04.017
dc.identifier.pmid29768179
dc.identifier.urihttp://hdl.handle.net/20.500.14038/36512
dc.description.abstractRegulated antimicrobial peptide expression in the intestinal epithelium is key to defense against infection and to microbiota homeostasis. Understanding the mechanisms that regulate such expression is necessary for understanding immune homeostasis and inflammatory disease and for developing safe and effective therapies. We used Caenorhabditis elegans in a preclinical approach to discover mechanisms of antimicrobial gene expression control in the intestinal epithelium. We found an unexpected role for the cholinergic nervous system. Infection-induced acetylcholine release from neurons stimulated muscarinic signaling in the epithelium, driving downstream induction of Wnt expression in the same tissue. Wnt induction activated the epithelial canonical Wnt pathway, resulting in the expression of C-type lectin and lysozyme genes that enhanced host defense. Furthermore, the muscarinic and Wnt pathways are linked by conserved transcription factors. These results reveal a tight connection between the nervous system and the intestinal epithelium, with important implications for host defense, immune homeostasis, and cancer.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=29768179&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5959051/
dc.subjectCaenorhabditis elegans
dc.subjectStaphylococcus aureus
dc.subjectWnt
dc.subjectcholinergic
dc.subjecthost defense
dc.subjectinfection
dc.subjectinnate immunity
dc.subjectintestinal epithelium
dc.subjectmuscarinic
dc.subjectnervous system
dc.subjectImmunology and Infectious Disease
dc.subjectMicrobiology
dc.titleIntestinal Epithelial Wnt Signaling Mediates Acetylcholine-Triggered Host Defense against Infection
dc.typeJournal Article
dc.source.journaltitleImmunity
dc.source.volume48
dc.source.issue5
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/maps_pubs/72
dc.identifier.contextkey16817187
html.description.abstract<p>Regulated antimicrobial peptide expression in the intestinal epithelium is key to defense against infection and to microbiota homeostasis. Understanding the mechanisms that regulate such expression is necessary for understanding immune homeostasis and inflammatory disease and for developing safe and effective therapies. We used Caenorhabditis elegans in a preclinical approach to discover mechanisms of antimicrobial gene expression control in the intestinal epithelium. We found an unexpected role for the cholinergic nervous system. Infection-induced acetylcholine release from neurons stimulated muscarinic signaling in the epithelium, driving downstream induction of Wnt expression in the same tissue. Wnt induction activated the epithelial canonical Wnt pathway, resulting in the expression of C-type lectin and lysozyme genes that enhanced host defense. Furthermore, the muscarinic and Wnt pathways are linked by conserved transcription factors. These results reveal a tight connection between the nervous system and the intestinal epithelium, with important implications for host defense, immune homeostasis, and cancer.</p>
dc.identifier.submissionpathmaps_pubs/72
dc.contributor.departmentDepartment of Microbiology and Physiological Systems
dc.source.pages963-978.e3


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