Salmonella enterica mediated epigenetic promotion of fibrosis is a novel factor in benign prostatic hyperplasia

作者：Cong Zhu, Luyao Li, Minghui Shi, Cheng Fang, Yang Lü, Ting Li, Fei Li, Shi-Song Yang, Tiankun Wang, Dao‐Jing Ming, Tong Deng, Haoyue Sun, Wenting Li, Jia Zhang, Yusen Zhang, Zhiyuan Jian, Changjiang Qin, Shuang-Ying Wang, Xian‐Tao Zeng · 发表于：Military Medical Research · 年份：2025 · DOI：10.1186/s40779-025-00614-2 · 被引用次数：3 · 研究领域：Ferroptosis and cancer prognosis、Bladder and Urothelial Cancer Treatments、Selenium in Biological Systems

Abstract Background Fibrosis constitutes a significant pathophysiological mechanism in the clinical progression of benign prostatic hyperplasia (BPH) and represents a contributing factor to the ineffectiveness of prevailing pharmacological treatments. Emerging evidence suggests a close association between microbial presence and the development of fibrosis. Nonetheless, the potential involvement of microbes within prostatic tissue in the pathogenesis of BPH and prostatic fibrosis, along with the underlying mechanisms, remains unexplored. Methods Utilizing immunohistochemistry and microbial sequencing, we analyzed the microbes of prostate tissues from BPH patients with different degrees of prostate fibrosis and found that Salmonella enterica ( S. enterica ) was enriched in the high degree of prostate fibrosis. We developed prostate cell and animal models infected with the lipopolysaccharide of S. enterica ( S.e -LPS) to assess its impact on prostate fibrosis. To elucidate the underlying functional mechanisms, we employed molecular biology techniques, including RNA degradation assays, N 6 -methyladenosine (m 6 A) dot blotting, RNA immunoprecipitation, and m 6 A immunoprecipitation. Results Microbial diversity differed between low- and high-fibrosis groups, with S. enterica showing the highest mean abundance among the four species that differed significantly. S.e -LPS was detected in S. enterica -rich prostate tissue and was found to significantly promote cell proliferation, cell...