CGRPβ suppresses the pathogenesis of ulcerative colitis via the immunoproteasome

Abstract Various factors have been implicated in the pathogenesis of ulcerative colitis (UC), with immune system failure being the most important one. Calcitonin gene-related peptide (CGRP), a neuropeptide with two isoforms, CGRPα and CGRPβ, has been reported to regulate the immune system. In this s...

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Main Authors: Tatsuya Shibao, Hiroaki Hase, Kodai Mizokami, Atsushi Usui, Kaori Kitae, Yuko Ueda, Kentaro Jingushi, Kazutake Tsujikawa
Format: Article
Language:English
Published: Nature Portfolio 2025-02-01
Series:Scientific Reports
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Online Access:https://doi.org/10.1038/s41598-025-91933-w
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author Tatsuya Shibao
Hiroaki Hase
Kodai Mizokami
Atsushi Usui
Kaori Kitae
Yuko Ueda
Kentaro Jingushi
Kazutake Tsujikawa
author_facet Tatsuya Shibao
Hiroaki Hase
Kodai Mizokami
Atsushi Usui
Kaori Kitae
Yuko Ueda
Kentaro Jingushi
Kazutake Tsujikawa
author_sort Tatsuya Shibao
collection DOAJ
description Abstract Various factors have been implicated in the pathogenesis of ulcerative colitis (UC), with immune system failure being the most important one. Calcitonin gene-related peptide (CGRP), a neuropeptide with two isoforms, CGRPα and CGRPβ, has been reported to regulate the immune system. In this study, we investigated the role of CGRP isoforms in UC pathogenesis. We induced UC-like symptoms in CGRPα and CGRPβ knockout (KO) mice using dextran sulphate sodium. Compared to wild-type and CGRPα KO mice, CGRPβ-deficient mice exhibited severe symptoms with increased blood in the stool and diarrhoea. Proteome analysis revealed significant up-regulation of immune-related proteins and immunoproteasome components in CGRPβ-deficient mice, suggesting that an enhanced immune response contributes to the severity of this disease. Treatment with ONX-0914, an immunoproteasome inhibitor, markedly improved these symptoms, highlighting the role of the immunoproteasome in exacerbating UC. This study provides the first evidence that CGRPβ protects against UC by modulating immune responses, particularly those mediated by the immunoproteasome. Our findings suggest that functional differences in CGRP isoforms may influence the severity and management of UC. This insight into the neuro-immune mechanism of UC opens avenues for novel therapies that address both the neural and immune aspects of this disease.
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spelling doaj-art-3bd73cae5cfe4c07add26dad06b3465d2025-08-20T03:04:20ZengNature PortfolioScientific Reports2045-23222025-02-0115111210.1038/s41598-025-91933-wCGRPβ suppresses the pathogenesis of ulcerative colitis via the immunoproteasomeTatsuya Shibao0Hiroaki Hase1Kodai Mizokami2Atsushi Usui3Kaori Kitae4Yuko Ueda5Kentaro Jingushi6Kazutake Tsujikawa7Laboratory of Molecular and Cellular Physiology, Graduate School of Pharmaceutical Sciences, Osaka UniversityLaboratory of Molecular and Cellular Physiology, Graduate School of Pharmaceutical Sciences, Osaka UniversityLaboratory of Molecular and Cellular Physiology, Graduate School of Pharmaceutical Sciences, Osaka UniversityLaboratory of Molecular and Cellular Physiology, Graduate School of Pharmaceutical Sciences, Osaka UniversityLaboratory of Molecular and Cellular Physiology, Graduate School of Pharmaceutical Sciences, Osaka UniversityLaboratory of Molecular and Cellular Physiology, Graduate School of Pharmaceutical Sciences, Osaka UniversityLaboratory of Molecular and Cellular Physiology, Graduate School of Pharmaceutical Sciences, Osaka UniversityLaboratory of Molecular and Cellular Physiology, Graduate School of Pharmaceutical Sciences, Osaka UniversityAbstract Various factors have been implicated in the pathogenesis of ulcerative colitis (UC), with immune system failure being the most important one. Calcitonin gene-related peptide (CGRP), a neuropeptide with two isoforms, CGRPα and CGRPβ, has been reported to regulate the immune system. In this study, we investigated the role of CGRP isoforms in UC pathogenesis. We induced UC-like symptoms in CGRPα and CGRPβ knockout (KO) mice using dextran sulphate sodium. Compared to wild-type and CGRPα KO mice, CGRPβ-deficient mice exhibited severe symptoms with increased blood in the stool and diarrhoea. Proteome analysis revealed significant up-regulation of immune-related proteins and immunoproteasome components in CGRPβ-deficient mice, suggesting that an enhanced immune response contributes to the severity of this disease. Treatment with ONX-0914, an immunoproteasome inhibitor, markedly improved these symptoms, highlighting the role of the immunoproteasome in exacerbating UC. This study provides the first evidence that CGRPβ protects against UC by modulating immune responses, particularly those mediated by the immunoproteasome. Our findings suggest that functional differences in CGRP isoforms may influence the severity and management of UC. This insight into the neuro-immune mechanism of UC opens avenues for novel therapies that address both the neural and immune aspects of this disease.https://doi.org/10.1038/s41598-025-91933-wCGRPUlcerative colitisImmunoproteasomeProteomics
spellingShingle Tatsuya Shibao
Hiroaki Hase
Kodai Mizokami
Atsushi Usui
Kaori Kitae
Yuko Ueda
Kentaro Jingushi
Kazutake Tsujikawa
CGRPβ suppresses the pathogenesis of ulcerative colitis via the immunoproteasome
Scientific Reports
CGRP
Ulcerative colitis
Immunoproteasome
Proteomics
title CGRPβ suppresses the pathogenesis of ulcerative colitis via the immunoproteasome
title_full CGRPβ suppresses the pathogenesis of ulcerative colitis via the immunoproteasome
title_fullStr CGRPβ suppresses the pathogenesis of ulcerative colitis via the immunoproteasome
title_full_unstemmed CGRPβ suppresses the pathogenesis of ulcerative colitis via the immunoproteasome
title_short CGRPβ suppresses the pathogenesis of ulcerative colitis via the immunoproteasome
title_sort cgrpβ suppresses the pathogenesis of ulcerative colitis via the immunoproteasome
topic CGRP
Ulcerative colitis
Immunoproteasome
Proteomics
url https://doi.org/10.1038/s41598-025-91933-w
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