Anti-Inflammatory Effect of Dialyzable Leukocyte Extract in Autoimmune Prostatitis: Evaluation in Animal Model.

Carlos Pérez-Alvarado,Miguel Reyes,Carlos Pérez De La Mora,Virginia Sanchez,D Guillermo Pérez Ishiwara,Consuelo Gómez,Mario García,Elizabeth Pérez

doi:10.1155/2017/1832853

Abstract

Objective. To evaluate the anti-inflammatory properties of Dialyzable Leukocyte Extract (DLE) in a murine model of chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). Methods. Histopathological characterization, prostatein Enzyme-Linked Immunosorbent Assay, and immunohistochemical analysis for CD45, TNF-α, IFN-γ, IL-6, IL-17, and IL-4 molecules were done in prostatic Wistar rats treated with DLE, placebo, or Dexamethasone. Results. Histopathological analysis of animals induced to prostatitis showed inflammatory infiltrate, mainly constituted by leucocytes and mast cells as well as Benign Prostatic Hyperplasia. Serum prostatein concentrations were 14 times higher than those displayed by healthy animals. After DLE and Dexamethasone treatments, the inflammatory infiltrate decreased; the tissue morphology was similar to that of a normal prostate, and the prostatein decreased to the basal levels of healthy animals. DLE treatment produced a decreased expression of the cell surface marker CD45 and the proinflammatory cytokines TNF-α, IFN-γ, IL-6, and IL-17. On the other hand, the expression of anti-inflammatory cytokine IL-4 increased in both the Dexamethasone and DLE groups. Conclusion. DLE is able to modulate the inflammatory response in Experimental Autoimmune Prostatitis (EAP).

Highlights

Prostatitis affects 10–20% of men from all ages and ethnic groups
Dialyzable Leukocyte Extract (DLE) is able to modulate the inflammatory response in Experimental Autoimmune Prostatitis (EAP)
The constant inflammation in chronic prostatitis could be related to Benign Prostatic Hyperplasia (BPH) development or even more to prostatic cancer (PC) [1]

Summary

Introduction

The chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) comprises more than 90% of all cases [1, 2]. Several authors suggest that CP/CPPS could be related to an autoimmune response [1]. In a murine model of prostatitis, prostate-specific autoantibodies as well as NO, TNF-α, and IFN-γ in seminal plasma were elevated [5]. All these data suggest that CP/CPPS may have, in part, autoimmune etiopathogenic features that involve an immune response against prostate-specific antigens, thereby tending to prolong a chronic inflammation status [5, 6]. The constant inflammation in chronic prostatitis could be related to Benign Prostatic Hyperplasia (BPH) development or even more to prostatic cancer (PC) [1]

Methods

Discussion

Conclusion