© 2007 THE AUTHORS JOURNAL COMPILATION © 2 0 0 7 B J U I N T E R N A T I O N A L | 1 0 0 , 7 3 3 – 7 3 7 | doi:10.1111/j.1464-410X.2007.07091.x 733 Mini Reviews INFLAMMATION AND INFECTION IN THE PATHOGENESIS OF PROSTATE CARCINOMA WAGENLEHNER et al. The role of inflammation and infection in the pathogenesis of prostate carcinoma Florian M.E. Wagenlehner, Johny E. Elkahwaji*, Ferran Algaba†, Truls Bjerklund-Johansen‡, Kurt G. Naber¶, Rudolf Hartung§ and Wolfgang Weidner Department of Urology, Justus-Liebig-University Giessen, Germany, *Department of Surgery, Division of Urological Surgery, University of Nebraska Medical Center, Omaha, USA, †Department of Pathology, Fundacio Puigvert, Barcelona, Spain, ‡Department of Urology, Telemark Hospital, Porsgrunn, Norway, ¶Technische Universität, München, and §Department of Urology, der Technischen Universität Munich, Klinikum rechts der Isar, Munich, Germany Accepted for publication 13 April 2007 Prostatitis and prostate carcinoma are both frequent entities of prostatic diseases. Epidemiological studies show significant associations between infection and inflammation and prostatic carcinoma. However, because of various confounding factors the results of these studies are inconclusive. Further findings are therefore needed to confirm the hypothesis that prostatic infection and inflammation might be a cause of prostatic carcinoma. We reviewed selected reports on the role of inflammation and infection in the pathogenesis of prostate carcinoma. Extensive genetic analyses show that several gene products, e.g. 2 ′ -5 ′ -oligoadenylate (2–5 A)-dependent Rnase, macrophage scavenger receptor 1 and Toll-like receptor-4, influence the susceptibility of prostate cells to infectious agents. Proliferative inflammatory atrophy (PIA) could be a connection between prostatitis and prostatic carcinoma. In the transition from PIA to prostatic intraepithelial neoplasia, the function of cellular detoxification is gradually lost by silencing of glutathione-S transferase, a detoxifying enzyme. This cellular feature leads to an increased susceptibility of the prostatic epithelial cells to genomic damage by inflammatory oxidants or nutritional carcinogens. Consecutive somatic genome damage might then arise which modulates the further pathogenesis of prostate carcinoma. Summarising these epidemiological, genetic and cell biological aspects, infectious prostatitis might have a causative role in the complex and multifactorial process of prostate carcinogenesis. KEYWORDS prostatic carcinoma, prostatitis, genetic susceptibility, proliferative inflammatory atrophy INTRODUCTION Chronic inflammation and chronic infection influences the emergence of various human neoplasms; the inflammatory process causes repeated cell and genome damage which leads to increased cell proliferation. If an Two of the mini reviews are about aspects of prostate cancer that are currently often discussed. The role of inflammation in the pathogenesis of prostate cancer is of great interest and has led to many important changes in our approaches to the subject of prostate cancer. Intermittent androgen deprivation has been an alternative therapeutic option for some time, but the absence of a large multicentre randomized controlled trial has delayed its general acceptance; this is discussed in detail in this section.