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ORIGINAL RESEARCH article

Front. Immunol.
Sec. Autoimmune and Autoinflammatory Disorders: Autoinflammatory Disorders
Volume 15 - 2024 | doi: 10.3389/fimmu.2024.1413078
This article is part of the Research Topic Novel Mechanisms Involved in Urinary Bladder Control: Advances in Neural, Humoral and Local Factors Underlying Function and Disease, Volume III View all 8 articles

PACAP/PAC1 Regulation in Cystitis Rats: Induction of Bladder Inflammation Cascade Leading to Bladder Dysfunction

Provisionally accepted
Hanwei Ke Hanwei Ke 1*Lin Zhu Lin Zhu 2*Weiyu Zhang Weiyu Zhang 1*Huanrui Wang Huanrui Wang 1Zehua Ding Zehua Ding 1*Dongyu Su Dongyu Su 1*Qi Wang Qi Wang 1*Kexin Xu Kexin Xu 1*
  • 1 Peking University People's Hospital, Beijing, China
  • 2 Beijing Chaoyang Hospital, Capital Medical University, Beijing, Beijing Municipality, China

The final, formatted version of the article will be published soon.

    Abstract This study explores the role of Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP) and its receptor, PAC1, in the pathophysiology of Interstitial Cystitis/Bladder Pain Syndrome (IC/BPS), a chronic condition marked by bladder pain and urinary urgency. Analysis of bladder tissue from IC/BPS patients and a rat model of cystitis revealed a significant increase in PACAP expression, which correlated with heightened inflammation and bladder dysfunction. We employed transcriptomic analysis, immunohistochemistry, and bladder function assays to investigate the role of the PACAP/PAC1 pathway in inflammation and sensory perception. The findings indicate that PACAP and PAC1 are significantly upregulated in IC/BPS, contributing to bladder inflammation and changes in sensory functions. Modulation of this pathway in rats led to reduced inflammation and improved bladder function, suggesting that the PACAP/PAC1 pathway could serve as a therapeutic target for IC/BPS.

    Keywords: interstitial cystitis, bladder pain syndrome, PACAP, PAC1 receptor, bladder inflammation

    Received: 06 Apr 2024; Accepted: 08 Nov 2024.

    Copyright: © 2024 Ke, Zhu, Zhang, Wang, Ding, Su, Wang and Xu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Hanwei Ke, Peking University People's Hospital, Beijing, China
    Lin Zhu, Beijing Chaoyang Hospital, Capital Medical University, Beijing, 100001, Beijing Municipality, China
    Weiyu Zhang, Peking University People's Hospital, Beijing, China
    Zehua Ding, Peking University People's Hospital, Beijing, China
    Dongyu Su, Peking University People's Hospital, Beijing, China
    Qi Wang, Peking University People's Hospital, Beijing, China
    Kexin Xu, Peking University People's Hospital, Beijing, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.