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

Author

Listed:
  • 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
    Department of Cancer Biology, Meharry Medical College)

  • Renyuan Zhang

    (Department of Cancer Genetics and Genomics, Roswell Park Comprehensive Cancer Center)

  • Nadia A. Lanman

    (Purdue University
    Purdue University)

  • Brittany Lapin

    (NorthShore University HealthSystem
    Department of Quantitative Health Sciences, Lerner Research Institute, Cleveland Clinic)

  • 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
    Mie University Graduate School of Medicine)

  • Gregory M. Cresswell

    (Purdue University
    The George Washington University)

  • Meaghan M. Broman

    (Purdue University)

  • J. Sebastian Paez

    (Purdue University
    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
    NorthShore University HealthSystem)

  • Omar E. Franco

    (an Academic Affiliate of the University of Chicago Pritzker School of Medicine)

  • Timothy L. Ratliff

    (Purdue University
    Purdue University)

  • Kent L. Nastiuk

    (Department of Cancer Genetics and Genomics, Roswell Park Comprehensive Cancer Center
    Department of Urology, 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)

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.

Suggested Citation

  • 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 Pae, 2022. "TNF is a potential therapeutic target to suppress prostatic inflammation and hyperplasia in autoimmune disease," Nature Communications, Nature, vol. 13(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:13:y:2022:i:1:d:10.1038_s41467-022-29719-1
    DOI: 10.1038/s41467-022-29719-1
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    References listed on IDEAS

    as
    1. Julius Gudmundsson & Jon K. Sigurdsson & Lilja Stefansdottir & Bjarni A. Agnarsson & Helgi J. Isaksson & Olafur A. Stefansson & Sigurjon A. Gudjonsson & Daniel F. Gudbjartsson & Gisli Masson & Michael, 2018. "Genome-wide associations for benign prostatic hyperplasia reveal a genetic correlation with serum levels of PSA," Nature Communications, Nature, vol. 9(1), pages 1-8, December.
    2. Jianming Zhang & Lingyu Fu & Jingpu Shi & Xin Chen & Yongze Li & Bing Ma & Yao Zhang, 2013. "The Risk of Metabolic Syndrome in Patients with Rheumatoid Arthritis: A Meta-Analysis of Observational Studies," PLOS ONE, Public Library of Science, vol. 8(10), pages 1-1, October.
    3. Bianca Cioni & Anniek Zaalberg & Judy R. Beijnum & Monique H. M. Melis & Johan Burgsteden & Mauro J. Muraro & Erik Hooijberg & Dennis Peters & Ingrid Hofland & Yoni Lubeck & Jeroen Jong & Joyce Sander, 2020. "Androgen receptor signalling in macrophages promotes TREM-1-mediated prostate cancer cell line migration and invasion," Nature Communications, Nature, vol. 11(1), pages 1-17, December.
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