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

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 and Simon W. Hayward ()
Additional contact information
Renee E. Vickman: an Academic Affiliate of the University of Chicago Pritzker School of Medicine
LaTayia Aaron-Brooks: an Academic Affiliate of the University of Chicago Pritzker School of Medicine
Renyuan Zhang: Department of Cancer Genetics and Genomics, Roswell Park Comprehensive Cancer Center
Nadia A. Lanman: Purdue University
Brittany Lapin: NorthShore University HealthSystem
Victoria Gil: an Academic Affiliate of the University of Chicago Pritzker School of Medicine
Max Greenberg: an Academic Affiliate of the University of Chicago Pritzker School of Medicine
Takeshi Sasaki: an Academic Affiliate of the University of Chicago Pritzker School of Medicine
Gregory M. Cresswell: Purdue University
Meaghan M. Broman: Purdue University
J. Sebastian Paez: Purdue University
Jacqueline Petkewicz: an Academic Affiliate of the University of Chicago Pritzker School of Medicine
Pooja Talaty: an Academic Affiliate of the University of Chicago Pritzker School of Medicine
Brian T. Helfand: an Academic Affiliate of the University of Chicago Pritzker School of Medicine
Alexander P. Glaser: an Academic Affiliate of the University of Chicago Pritzker School of Medicine
Chi-Hsiung Wang: an Academic Affiliate of the University of Chicago Pritzker School of Medicine
Omar E. Franco: an Academic Affiliate of the University of Chicago Pritzker School of Medicine
Timothy L. Ratliff: Purdue University
Kent L. Nastiuk: Department of Cancer Genetics and Genomics, Roswell Park Comprehensive Cancer Center
Susan E. Crawford: an Academic Affiliate of the University of Chicago Pritzker School of Medicine
Simon W. Hayward: an Academic Affiliate of the University of Chicago Pritzker School of Medicine

Nature Communications, 2022, vol. 13, issue 1, 1-15

Abstract: 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 to evaluate the impact of inflammation, as seen in AI diseases, on prostate tissue. Human and mouse tissues are used to examine whether systemic targeting of inflammation limits prostatic inflammation and hyperplasia. Evaluation of 112,152 medical records indicates that benign prostatic hyperplasia (BPH) prevalence is significantly higher among patients with AI diseases. Furthermore, treating these patients with tumor necrosis factor (TNF)-antagonists significantly decreases BPH incidence. Single-cell RNA-seq and in vitro assays suggest that macrophage-derived TNF stimulates BPH-derived fibroblast proliferation. TNF blockade significantly reduces epithelial hyperplasia, NFκB activation, and macrophage-mediated inflammation within prostate tissues. Together, these studies show that patients with AI diseases have a heightened susceptibility to BPH and that reducing inflammation with a therapeutic agent can suppress BPH.

Date: 2022
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DOI: 10.1038/s41467-022-29719-1

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