Cathelicidins Induce Toll-Interacting Protein Synthesis to Prevent Apoptosis in Colonic Epithelium
Cathelicidin peptides secreted by leukocytes and epithelial cells are microbicidal but also regulate pathogen sensing via toll-like receptors (TLRs) in the colon by mechanisms that are not fully understood. Herein, analyses with the attaching/effacing pathogen Citrobacter rodentium model of colitis in cathelicidin-deficient (Camp−/−) mice, and colonic epithelia demonstrate that cathelicidins prevent apoptosis by sustaining post-transcriptional synthesis of a TLR adapter, toll-interacting protein (TOLLIP). Cathelicidins induced phosphorylation-activation of epidermal growth factor receptor (EGFR)-kinase, which phosphorylated-inactivated miRNA-activating enzyme Argonaute 2 (AGO2), thus reducing availability of the TOLLIP repressor miRNA-31. Cathelicidins promoted stability of TOLLIP protein via a proteosome-dependent pathway. This cathelicidin-induced TOLLIP upregulation prevented apoptosis in the colonic epithelium by reducing levels of caspase-3 and poly (ADP-ribose) polymerase (PARP)-1 in response to the proinflammatory cytokines, interferon-γ (IFNγ) and tumor necrosis factor-α (TNFα). Further, Camp−/− colonic epithelial cells were more susceptible to apoptosis during C. rodentium infection than wild-type cells. This antiapoptotic effect of cathelicidins, maintaining epithelial TOLLIP protein in the gut, provides insight into cathelicidin’s ability to regulate TLR signaling and prevent exacerbated inflammation.
- Standort
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Deutsche Nationalbibliothek Frankfurt am Main
- Umfang
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Online-Ressource
- Sprache
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Englisch
- Erschienen in
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Cathelicidins Induce Toll-Interacting Protein Synthesis to Prevent Apoptosis in Colonic Epithelium ; volume:15 ; number:1 ; year:2022 ; pages:204-221 ; extent:18
Journal of innate immunity ; 15, Heft 1 (2022), 204-221 (gesamt 18)
- Urheber
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Holani, Ravi
Rathnayaka, Chathurika
Blyth, Graham A.D.
Babbar, Anshu
Lahiri, Priyoshi
Young, Daniel
Dufour, Antoine
Hollenberg, Morley D.
McKay, Derek M.
Cobo, Eduardo R.
- DOI
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10.1159/000526121
- URN
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urn:nbn:de:101:1-2024010323525758125633
- Rechteinformation
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Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Letzte Aktualisierung
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15.08.2025, 07:38 MESZ
Datenpartner
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Beteiligte
- Holani, Ravi
- Rathnayaka, Chathurika
- Blyth, Graham A.D.
- Babbar, Anshu
- Lahiri, Priyoshi
- Young, Daniel
- Dufour, Antoine
- Hollenberg, Morley D.
- McKay, Derek M.
- Cobo, Eduardo R.
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