TNF is a potential therapeutic target to suppress prostatic inflammation and hyperplasia in autoimmune disease

• DOI: 10.1038/s41467-022-29719-1
• Publication Date: 2022-04-19T10:03:39Z
• Authors: Renee E. Vickman; LaTayia Aaron-Brooks; Renyuan Zhang; Nadia A. Lanman; Brittany Lapin; Victoria Gil; Max Greenberg; Takeshi Sasaki; Gregory M. Cresswell; Meaghan M. Broman; J. Sebastian Paez; Jacqueline Petkewicz; Pooja Talaty; Brian T. Helfand; Alexander P. Glaser; Chi-Hsiung Wang; Omar E. Franco; Timothy L. Ratliff; Kent L. Nastiuk; Susan E. Crawford; Simon W. Hayward
• Keywords: Inflammation; Male; Hyperplasia; Science; Q; Prostatic Hyperplasia; 610; Article; Autoimmune Diseases; Cell Line; Prostatitis; 3. Good health; Mice; Animals; Humans

Abstract Autoimmune (AI) diseases can affect many organs; however, the prostate has not been considered to be a primary target of these systemic inflammatory processes. Here, we utilize medical record data, patient samples, and in vivo models evaluate impact inflammation, as seen AI diseases, on tissue. Human mouse tissues are used examine whether targeting inflammation limits prostatic hyperplasia. Evaluation 112,152 records indicates that benign hyperplasia (BPH) prevalence is significantly higher among patients with diseases. Furthermore, treating tumor necrosis factor (TNF)-antagonists decreases BPH incidence. Single-cell RNA-seq vitro assays suggest macrophage-derived TNF stimulates BPH-derived fibroblast proliferation. blockade reduces epithelial hyperplasia, NFκB activation, macrophage-mediated within tissues. Together, studies show have heightened susceptibility reducing therapeutic agent suppress BPH.