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    Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/34632


    標題: EBV infection mediated BDNF expression is associated with bladder inflammation in interstitial cystitis/bladder pain syndrome with Hunner's lesion
    作者: Jhang, Jia-Fong
    Liu, Cheng-Der
    Hsu, Yung-Hsiang
    Chen, Chien-Chin
    Chen, Hsiang-Chin
    Jiang, Yuan-Hong
    Wu, Wan-Chen
    Peng, Chih-Wen
    Kuo, Hann-Chorng
    貢獻者: Buddhist Tzu Chi General Hospital
    Hualien Tzu Chi Hospital
    Tzu Chi University
    National Dong Hwa University
    Buddhist Tzu Chi General Hospital
    Hualien Tzu Chi Hospital
    Tzu Chi University
    Department of Cosmetic Science, Chia Nan University of Pharmacy & Science
    National Cheng Kung University
    Buddhist Tzu Chi General Hospital
    Hualien Tzu Chi Hospital
    關鍵字: botulinum-toxin-a
    syndrome/interstitial cystitis
    neurotrophic factor
    cell-line
    coactivation
    identification
    prevalence
    promoter
    binding
    trkb
    日期: 2023
    上傳時間: 2023-12-11 14:01:39 (UTC+8)
    出版者: WILEY
    摘要: Interstitial cystitis/bladder pain syndrome with Hunner's lesion (HIC) is characterized by chronic inflammation and nerve hyperplasia; however, the pathogenesis of HIC remains a mystery. In this study, we detected both Epstein-Barr virus (EBV) latency infection genes EBNA-1 and LMP-1 and EBV lytic infection BZLF-1 and BRLF-1 expression in the HIC bladders, indicating the coexistence of EBV persistence and reactivation in the B cells in HIC bladders. Upregulation of EBV-associated inflammatory genes in HIC bladders, such as TNF-alpha and IL-6, suggests EBV infection is implicated in the pathogenesis of bladder inflammation. Nerve hyperplasia and upregulation of brain-derived neurotrophic factor (BDNF) were noted in the HIC bladders. Double immunochemical staining and flow cytometry revealed the origin of BDNF to be EBV-infected B cells. Inducible BDNF expression was noted in B cells upon EBV infection, but not in the T cells. A chromatin immunoprecipitation study revealed BDNF transcription could be promoted by cooperation between EBV nuclear antigens, chromatin modifiers, and B-cell-specific transcription. Knockdown of BDNF in EBV-infected B cells resulted in the inhibition of cell proliferation and viability. Downregulation of phosphorylated SMAD2 and STAT3 after BDNF knockdown may play a role in the mechanism. Implantation of latent EBV-infected B cells into rat bladder walls resulted in a higher expression level of CD45 and PGP9.5, suggesting tissue inflammation and nerve hyperplasia. In contrast, implantation of BDNF depleted EBV-infected B cells abrogated these effects. This is the first study to provide insights into the mechanisms underlying the involvement of EBV-infected B cells in HIC pathogenesis. (c) 2022 The Pathological Society of Great Britain and Ireland.
    關聯: Journal of Pathology, v.259, n.3, pp.276-290
    Appears in Collections:[化妝品應用與管理系(所)] 期刊論文

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