From clinical observations to molecular insights: Decoding immune checkpoint inhibitors‐induced prostatitis

Abstract Immune checkpoint inhibitors (ICIs) have dramatically transformed cancer treatment; however, their impact on the male reproductive system remains poorly understood. This study aims to elucidate the incidence, risk factors, and molecular mechanisms underlying ICI‐associated prostatitis. We c...

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Main Authors: Peng Luo, Ying Liu, Lan Xu, Zaoqu Liu, Linhui Wang, Hank Z. H. Wong, Quan Cheng, Anqi Lin, Xiao Fang, Aimin Jiang
Format: Article
Language:English
Published: Wiley 2025-06-01
Series:View
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Online Access:https://doi.org/10.1002/VIW.20240113
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author Peng Luo
Ying Liu
Lan Xu
Zaoqu Liu
Linhui Wang
Hank Z. H. Wong
Quan Cheng
Anqi Lin
Xiao Fang
Aimin Jiang
author_facet Peng Luo
Ying Liu
Lan Xu
Zaoqu Liu
Linhui Wang
Hank Z. H. Wong
Quan Cheng
Anqi Lin
Xiao Fang
Aimin Jiang
author_sort Peng Luo
collection DOAJ
description Abstract Immune checkpoint inhibitors (ICIs) have dramatically transformed cancer treatment; however, their impact on the male reproductive system remains poorly understood. This study aims to elucidate the incidence, risk factors, and molecular mechanisms underlying ICI‐associated prostatitis. We conducted an analysis of ICI‐associated prostatitis utilizing the U.S. Food and Drug Administration Adverse Event Reporting System (FAERS) database and evaluated risk through the application of the reporting odds ratio. A mouse model of ICI treatment was developed, and subsequent transcriptomic changes in prostate tissue were investigated using high‐throughput sequencing. Hematoxylin and eosin staining, immunohistochemistry, Von Frey testing, and enzyme‐linked immunosorbent assay were employed to confirm ICI‐induced prostatitis and further delineate its underlying mechanisms. Additionally, we investigated the therapeutic potential of specifically targeting interleukin‐6 (IL‐6) and extracellular signal‐regulated kinase (ERK) signaling pathways. FAERS analysis demonstrated a statistically significant positive correlation between ICI treatment and prostatitis risk (p < .05). In the murine model, ICI treatment induced an elevated inflammatory response in prostate tissue, characterized by enhanced inflammatory cell infiltration and upregulated expression of IL‐6 and tumor necrosis factor‐alpha. Transcriptomic analysis revealed significant activation of multiple inflammation‐related signaling pathways in prostate tissue following ICI treatment (false discovery rate < 0.05). Targeted inhibition of IL‐6 or ERK signaling pathways significantly attenuated ICI‐induced prostatitis symptoms, resulting in improved tissue pathology and decreased inflammatory factor expression (p < .01). This study delineates the characteristics and potential molecular mechanisms underlying ICI‐associated prostatitis, thereby establishing a theoretical foundation for the development of prevention and treatment strategies. Targeted modulation of IL‐6 and ERK signaling pathways may present novel therapeutic interventions for ICI‐associated prostatitis, thus warranting further clinical validation.
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spelling doaj-art-853952f7c67140fea3ef68afe0160d202025-08-20T03:31:07ZengWileyView2688-39882688-268X2025-06-0163n/an/a10.1002/VIW.20240113From clinical observations to molecular insights: Decoding immune checkpoint inhibitors‐induced prostatitisPeng Luo0Ying Liu1Lan Xu2Zaoqu Liu3Linhui Wang4Hank Z. H. Wong5Quan Cheng6Anqi Lin7Xiao Fang8Aimin Jiang9Donghai County People's Hospital ‐ Jiangnan University Smart Healthcare Joint Laboratory Donghai County People's Hospital (Affiliated Kangda College of Nanjing Medical University) Lianyungang ChinaDepartment of Urology, Changhai Hospital Naval Medical University (Second Military Medical University) Shanghai ChinaDepartment of Oncology Zhujiang Hospital Southern Medical University Guangzhou ChinaInstitute of Basic Medical Sciences Chinese Academy of Medical Sciences and Peking Union Medical College Beijing ChinaDepartment of Urology, Changhai Hospital Naval Medical University (Second Military Medical University) Shanghai ChinaLi Ka Shing Faculty of Medicine The University of Hong Kong Hong Kong SAR ChinaDepartment of Neurosurgery Xiangya Hospital Central South University Changsha ChinaDonghai County People's Hospital ‐ Jiangnan University Smart Healthcare Joint Laboratory Donghai County People's Hospital (Affiliated Kangda College of Nanjing Medical University) Lianyungang ChinaDepartment of Urology, Changzheng Hospital Naval Medical University (Second Military Medical University) Shanghai ChinaDepartment of Urology, Changzheng Hospital Naval Medical University (Second Military Medical University) Shanghai ChinaAbstract Immune checkpoint inhibitors (ICIs) have dramatically transformed cancer treatment; however, their impact on the male reproductive system remains poorly understood. This study aims to elucidate the incidence, risk factors, and molecular mechanisms underlying ICI‐associated prostatitis. We conducted an analysis of ICI‐associated prostatitis utilizing the U.S. Food and Drug Administration Adverse Event Reporting System (FAERS) database and evaluated risk through the application of the reporting odds ratio. A mouse model of ICI treatment was developed, and subsequent transcriptomic changes in prostate tissue were investigated using high‐throughput sequencing. Hematoxylin and eosin staining, immunohistochemistry, Von Frey testing, and enzyme‐linked immunosorbent assay were employed to confirm ICI‐induced prostatitis and further delineate its underlying mechanisms. Additionally, we investigated the therapeutic potential of specifically targeting interleukin‐6 (IL‐6) and extracellular signal‐regulated kinase (ERK) signaling pathways. FAERS analysis demonstrated a statistically significant positive correlation between ICI treatment and prostatitis risk (p < .05). In the murine model, ICI treatment induced an elevated inflammatory response in prostate tissue, characterized by enhanced inflammatory cell infiltration and upregulated expression of IL‐6 and tumor necrosis factor‐alpha. Transcriptomic analysis revealed significant activation of multiple inflammation‐related signaling pathways in prostate tissue following ICI treatment (false discovery rate < 0.05). Targeted inhibition of IL‐6 or ERK signaling pathways significantly attenuated ICI‐induced prostatitis symptoms, resulting in improved tissue pathology and decreased inflammatory factor expression (p < .01). This study delineates the characteristics and potential molecular mechanisms underlying ICI‐associated prostatitis, thereby establishing a theoretical foundation for the development of prevention and treatment strategies. Targeted modulation of IL‐6 and ERK signaling pathways may present novel therapeutic interventions for ICI‐associated prostatitis, thus warranting further clinical validation.https://doi.org/10.1002/VIW.20240113FAERSICI‐associated prostatitisimmune checkpoint inhibitorsmolecular mechanismmurine model
spellingShingle Peng Luo
Ying Liu
Lan Xu
Zaoqu Liu
Linhui Wang
Hank Z. H. Wong
Quan Cheng
Anqi Lin
Xiao Fang
Aimin Jiang
From clinical observations to molecular insights: Decoding immune checkpoint inhibitors‐induced prostatitis
View
FAERS
ICI‐associated prostatitis
immune checkpoint inhibitors
molecular mechanism
murine model
title From clinical observations to molecular insights: Decoding immune checkpoint inhibitors‐induced prostatitis
title_full From clinical observations to molecular insights: Decoding immune checkpoint inhibitors‐induced prostatitis
title_fullStr From clinical observations to molecular insights: Decoding immune checkpoint inhibitors‐induced prostatitis
title_full_unstemmed From clinical observations to molecular insights: Decoding immune checkpoint inhibitors‐induced prostatitis
title_short From clinical observations to molecular insights: Decoding immune checkpoint inhibitors‐induced prostatitis
title_sort from clinical observations to molecular insights decoding immune checkpoint inhibitors induced prostatitis
topic FAERS
ICI‐associated prostatitis
immune checkpoint inhibitors
molecular mechanism
murine model
url https://doi.org/10.1002/VIW.20240113
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