PMID- 36979355
OWN - NLM
STAT- MEDLINE
DCOM- 20230330
LR  - 20230331
IS  - 2218-273X (Electronic)
IS  - 2218-273X (Linking)
VI  - 13
IP  - 3
DP  - 2023 Feb 23
TI  - Immunogenic Cell Death Associated Molecular Patterns and the Dual Role of IL17RA 
      in Interstitial Cystitis/Bladder Pain Syndrome.
LID - 10.3390/biom13030421 [doi]
LID - 421
AB  - The unclear etiology and pathogenesis of interstitial cystitis/bladder pain 
      syndrome (IC/BPS) are responsible for the lack of effective treatment and the 
      poor patient prognosis. Various studies show that chronic inflammation and immune 
      responses are important factors contributing to the pathogenesis of IC/BPS. The 
      process of immunogenic cell death (ICD) involves both the immune response and 
      inflammatory process, and the involvement of ICD in IC/BPS pathogenesis has not 
      been explored. Two IC/BPS transcriptome datasets collected from the Gene 
      Expression Omnibus (GEO) database were used to identify distinct ICD-associated 
      molecular patterns (IAMPs). IAMPs and IC/BPS subtypes were found to be related. 
      The inflammatory immune microenvironments (IIME) in different IAMPs were studied. 
      The potential mechanism by which the interleukin 17 receptor A (IL17RA) 
      influences IC/BPS was examined using in vitro assays. The expression of 
      ICD-related genes (IRGs) was upregulated in IC/BPS bladders, compared with normal 
      bladders. Disease prediction models, based on differentially expressed IRGs, 
      could accurately predict IC/BPS. The IC/BPS patients had two distinct IAMPs, each 
      with its own subtype and clinical features and association with remodeling IIME. 
      IL17RA, a well-established IC/BPS bladder biomarker, mediates both the 
      inflammatory insult and the protective responses. In summary, the current study 
      identified different IAMPs in IC/BPS, which may be involved in the pathogenesis 
      of IC/BPS by remodeling the IIME. The chronic inflammatory process in IC/BPS may 
      be prolonged by IL17RA, which could mediate both pro- and anti-inflammatory 
      responses. The IL17RA-associated pathway may play a significant role in the 
      development of IC/BPS and can be used as a therapeutic target.
FAU - Zhang, Wei
AU  - Zhang W
AUID- ORCID: 0000-0002-3167-0002
AD  - Department of Urology, Beijing Hospital, National Center of Gerontology, 
      Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing 
      100730, China.
FAU - Liu, Xiaodong
AU  - Liu X
AD  - Department of Urology, Beijing Hospital, National Center of Gerontology, 
      Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing 
      100730, China.
FAU - Wang, Jiawen
AU  - Wang J
AD  - Department of Urology, Beijing Hospital, National Center of Gerontology, 
      Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing 
      100730, China.
FAU - Wang, Xinhao
AU  - Wang X
AD  - Department of Urology, Beijing Hospital, National Center of Gerontology, 
      Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing 
      100730, China.
FAU - Zhang, Yaoguang
AU  - Zhang Y
AD  - Department of Urology, Beijing Hospital, National Center of Gerontology, 
      Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing 
      100730, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20230223
PL  - Switzerland
TA  - Biomolecules
JT  - Biomolecules
JID - 101596414
RN  - 0 (Receptors, Interleukin-17)
RN  - 0 (IL17RA protein, human)
SB  - IM
MH  - Humans
MH  - *Cystitis, Interstitial/genetics/metabolism/pathology
MH  - Receptors, Interleukin-17/genetics
MH  - Immunogenic Cell Death
MH  - Urinary Bladder/metabolism
MH  - Inflammation/genetics/pathology
PMC - PMC10046465
OTO - NOTNLM
OT  - immunogenic cell death
OT  - interleukin 17 receptor
OT  - interstitial cystitis
OT  - macrophages
OT  - urothelial cells
COIS- The authors declare no conflict of interest.
EDAT- 2023/03/30 06:00
MHDA- 2023/03/30 06:11
PMCR- 2023/02/23
CRDT- 2023/03/29 01:19
PHST- 2022/11/30 00:00 [received]
PHST- 2023/02/09 00:00 [revised]
PHST- 2023/02/14 00:00 [accepted]
PHST- 2023/03/30 06:11 [medline]
PHST- 2023/03/29 01:19 [entrez]
PHST- 2023/03/30 06:00 [pubmed]
PHST- 2023/02/23 00:00 [pmc-release]
AID - biom13030421 [pii]
AID - biomolecules-13-00421 [pii]
AID - 10.3390/biom13030421 [doi]
PST - epublish
SO  - Biomolecules. 2023 Feb 23;13(3):421. doi: 10.3390/biom13030421.