Time course of reactive oxygen intermediates release and histopathological findings during experimental autoimmune prostatitis development

Abstract

Spontaneous and stimulated reactive oxygen intermediates (ROI) release by peritoneal exudate cells (PEC) and histopathological findings in the prostate gland were assessed during experimental autoimmune prostatitis (EAP) development. Results in EAP rats were compared with data from rats immunized with kidney homogenate, BSA, and CFA, as well as nontreated rats. At 28 days of first immunization (FI), EAP rats spontaneously released significantly more ROI than occurred in the cells from control rats. A similar response was found when ROI release was analyzed after in vitro stimulus. In time course studies, an increased spontaneous O2- production was observed at day 7 after FI, and remained the same during all period studied, (14, 21, and 28 days after FI). The stimulated O2- production showed elevated levels at 7 days after FI and fell afterward to levels similar to those of nontreated rats and increased again at 28 days. Spontaneous or stimulated H2O2 release showed a progressive increase during the study periods. ROI release was correlated with infiltrate formation in the prostate gland. This differential responsiveness could indicate that, during the autoimmune process, the autoantigen(s) amplify the inflammatory response triggered by them.

Non-obese Diabetic (NOD) Mice are Genetically Susceptible to Experimental Autoimmune Prostatitis (EAP)

“…As in Wistar rats, MAG elicits both a humoral and a cell-mediated response in NOD mice. In the rat model, we have shown that the cell-mediated response gave rise to reactive oxygen intermediates and to CD8 + cytotoxic T cells, two agents potentially capable of causing tissue damage [12,13]. A future objective is to identify which of these effector agents are responsible for the destructive lesions seen in NOD mice and whether B cells and antibodies detected soon after immunization also participate in the pathogenic process.…”

“…EAP can be adoptively transferred into naïve Wistar rats by whole spleen cells of autoimmune donors, but not by spleen cells which have been depleted of T lymphocytes prior to transfer in vitro [11]. Pathogenic reactive oxygen intermediates released by macrophages [12] and cytotoxic T lymphocytes [13] have been demonstrated in diseased rats and may be responsible for tissue alterations observed on histological sections.…”

Prostatein or Steroid Binding Protein (PSBP) Induces Experimental Autoimmune Prostatitis (EAP) in NOD Mice

“…Both cytotoxic T lymphocytes and pathogenic reactive oxygen intermediates released by macrophages have been identified in diseased rats and are probably responsible for the tissue alterations observed on histological sections (6,7).…”

New therapy with XLQ® to suppress chronic prostatitis through its anti‐inflammatory and antioxidative activities

“…Although the exact mechanism of IL-17 in the regulation of inflammation and pain has not been proven, our Moreover, oxidative stress has been considered as a significant factor in the inflammatory cascade of chronic prostatitis evidenced by both in vitro and in vivo studies (Kullisaar, Turk, Punab, & Mandar, 2012;Polackwich & Shoskes, 2016;Pontari & Ruggieri, 2004). In early animal studies, reactive nitrogen intermediates and reactive oxygen intermediates were suggested to be of pathogenic importance in the development of early tissue inflammation and autoimmune disease of the prostate Orsilles, Donadio, & Depiante-Depaoli, 1995). In addition, in humans, it is speculated that oxidative stress may be a key factor in some men with CPPS that can be targeted with antioxidant therapy (Shahed & Shoskes, 2000).…”