EBV infection mediated BDNF expression is associated with bladder inflammation in interstitial cystitis/bladder pain syndrome with Hunner's lesion

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Title:	EBV infection mediated BDNF expression is associated with bladder inflammation in interstitial cystitis/bladder pain syndrome with Hunner's lesion
Authors:	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
Contributors:	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
Keywords:	botulinum-toxin-a syndrome/interstitial cystitis neurotrophic factor cell-line coactivation identification prevalence promoter binding trkb
Date:	2023
Issue Date:	2023-12-11 14:01:39 (UTC+8)
Publisher:	WILEY
Abstract:	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.
Relation:	Journal of Pathology, v.259, n.3, pp.276-290
Appears in Collections:	[Dept. of Cosmetic Science and institute of cosmetic science] Periodical Articles

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