Effect of alcohol on chronic pelvic pain and prostatic inflammation in a mouse model of experimental autoimmune prostatitis

The Prostate ◽  
2019 ◽  
Vol 79 (12) ◽  
pp. 1466-1476 ◽  
Author(s):  
Li‐Gang Zhang ◽  
Jing Chen ◽  
Jia‐Lin Meng ◽  
Yong Zhang ◽  
Yi Liu ◽  
...  
Keyword(s):  
Mouse Model ◽  
Pelvic Pain ◽  
Chronic Pelvic Pain ◽  
Prostatic Inflammation ◽  
Experimental Autoimmune

Effect of tadalafil on chronic pelvic pain and prostatic inflammation in a rat model of experimental autoimmune prostatitis

The Prostate ◽  
2018 ◽  
Vol 78 (10) ◽  
pp. 707-713 ◽  
Author(s):  
Ken Okamoto ◽  
Maki Kurita ◽  
Hiroshi Yamaguchi ◽  
Yuki Numakura ◽  
Michiko Oka
Keyword(s):  
Pelvic Pain ◽  
Rat Model ◽  
Chronic Pelvic Pain ◽  
Prostatic Inflammation ◽  
Experimental Autoimmune

Effect of Eriocalyxin B on prostatic inflammation and pelvic pain in a mouse model of experimental autoimmune prostatitis

The Prostate ◽  
2020 ◽  
Vol 80 (16) ◽  
pp. 1394-1404
Author(s):  
Li‐Gang Zhang ◽  
Zi‐Qiang Yu ◽  
Cheng Yang ◽  
Jing Chen ◽  
Chang‐Sheng Zhan ◽  
...  
Keyword(s):  
Mouse Model ◽  
Pelvic Pain ◽  
Eriocalyxin B ◽  
Prostatic Inflammation ◽  
Experimental Autoimmune

Experimental autoimmune prostatitis induces chronic pelvic pain

2008 ◽  
Vol 294 (4) ◽  
pp. R1268-R1275 ◽  
Author(s):  
Charles N. Rudick ◽  
Anthony J. Schaeffer ◽  
Praveen Thumbikat
Keyword(s):  
Chronic Pain ◽  
Pelvic Pain ◽  
Chronic Pelvic Pain ◽  
Chronic Pelvic Pain Syndrome ◽  
Pain Syndrome ◽  
Pelvic Pain Syndrome ◽  
Protein Gene Product ◽  
Mouse Prostate ◽  
Inflammatory Infiltrates ◽  
Experimental Autoimmune

Pain is the hallmark of patients with chronic prostatitis (CP) and chronic pelvic pain syndrome (CPPS). Despite numerous hypotheses, the etiology and pathogenesis remain unknown. To better understand CP/CPPS, we used a murine experimental autoimmune prostatitis model to examine the development, localization, and modulation of pelvic pain. Pelvic pain was detected 5 days after antigen instillation and was sustained beyond 30 days, indicating the development of chronic pain. The pain was attenuated by lidocaine treatment into the prostate, but not into the bladder or the colon, suggesting that pain originated from the prostate. Experimental autoimmune prostatitis histopathology was confined to the prostate with focal periglandular inflammatory infiltrates in the ventral, dorsolateral, and anterior lobes of the mouse prostate. Inflammation and pelvic pain were positively correlated and increased with time. Morphologically, the dorsolateral prostate alone showed significantly increased neuronal fiber distribution, as evidenced by increased protein gene product 9.5 expression. Pelvic pain was attenuated by treatment with the neuromodulator gabapentin, suggesting spinal and/or supraspinal contribution to chronic pain. These results provide the basis for identifying mechanisms that regulate pelvic pain and the testing of therapeutic agents that block pain development in CP/CPPS.

scholarly journals Tryptase-PAR2 axis in experimental autoimmune prostatitis, a model for chronic pelvic pain syndrome

Pain ◽  
2014 ◽  
Vol 155 (7) ◽  
pp. 1328-1338 ◽  
Author(s):  
Kenny Roman ◽  
Joseph D. Done ◽  
Anthony J. Schaeffer ◽  
Stephen F. Murphy ◽  
Praveen Thumbikat
Keyword(s):  
Pelvic Pain ◽  
Chronic Pelvic Pain ◽  
Chronic Pelvic Pain Syndrome ◽  
Pain Syndrome ◽  
Pelvic Pain Syndrome ◽  
Experimental Autoimmune

scholarly journals CCL2 and CCL3 are essential mediators of pelvic pain in experimental autoimmune prostatitis

2012 ◽  
Vol 303 (6) ◽  
pp. R580-R589 ◽  
Author(s):  
Marsha L. Quick ◽  
Soumi Mukherjee ◽  
Charles N. Rudick ◽  
Joseph D. Done ◽  
Anthony J. Schaeffer ◽  
...  
Keyword(s):  
T Cells ◽  
Pelvic Pain ◽  
Neutralizing Antibodies ◽  
Chronic Pelvic Pain ◽  
Chronic Pelvic Pain Syndrome ◽  
Pain Syndrome ◽  
Pelvic Pain Syndrome ◽  
Pain Symptoms ◽  
Deficient Mice ◽  
Experimental Autoimmune

Experimental autoimmune prostatitis (EAP) is a murine model of chronic prostatitis/chronic pelvic pain syndrome (CPPS) in men, a syndrome characterized by chronic pelvic pain. We have demonstrated that chemokine ligands CCL2 and CCL3 are biomarkers that correlate with pelvic pain symptoms. We postulated that CCL2 and CCL3 play a functional role in CPPS and therefore examined their expression in EAP. Upon examination of the prostate 5 days after induction of EAP, CCL2 mRNA was elevated 2- to 3-fold, CCL8 by 15-fold, CCL12 by 12- to 13-fold, and CXCL9 by 2- to 4-fold compared with control mice. At 10 days the major chemokines were CXCL13 and CXCL2; at 20 days CCL2 (1- to 2-fold), CCL3 (2- to 3-fold) and CCL11 (2- to 3-fold); and at 30 days, CCL12 (20- to 35-fold) and smaller increases in CCL2, CCL3, and XCL1. Chemokine elevations were accompanied by increases in mast cells and B cells at 5 days, monocytes and neutrophils at day 10, CD4+ T cells at day 20, and CD4+ and CD8+ T cells at day 30. Anti-CCL2 and anti-CCL3 neutralizing antibodies administered at EAP onset attenuated pelvic pain development, but only anti-CCL2 antibodies were effective therapeutically. CCL2- and its cognate receptor CCR2-deficient mice were completely protected from development of pain symptoms but assumed susceptibility after reconstitution with wild-type bone marrow. CCL3-deficient mice showed resistance to the maintenance of pelvic pain while CCR5-deficient mice did not show any lessening of pelvic pain severity. These results suggest that the CCL2-CCR2 axis and CCL3 are important mediators of chronic pelvic pain in EAP.

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