Articles by Marsha L Quick in JoVE
Meting van Tactiele allodynie in een muizenmodel van bacteriële prostatitis Marsha L Quick1, Joseph D Done1, Praveen Thumbikat1 1Department of Urology, Northwestern University Feinberg School of Medicine Infectie van de prostaat kan een bijdragende factor in het bemiddelen bekken pijn bij chronische prostatitis zijn. We beschrijven de procedure voor het bereiden van gestandaardiseerde bacterieel inoculum, instillatie van bacteriën in de urethra van mannelijke muizen en methode voor het meten tactiele allodynie bij muizen in de tijd.
Other articles by Marsha L Quick on PubMed
Role of Mast Cells in Male Chronic Pelvic Pain The Journal of Urology. Apr, 2012 | Pubmed ID: 22341813 Chronic pelvic pain syndrome accounts for 90% of all chronic prostatitis but it has an unknown pathogenesis. We sought to understand the role of mast cells and nerve growth factor in chronic pelvic pain.
CCL2 and CCL3 Are Essential Mediators of Pelvic Pain in Experimental Autoimmune Prostatitis American Journal of Physiology. Regulatory, Integrative and Comparative Physiology. Sep, 2012 | Pubmed ID: 22814670 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.