Models of inflammation of the lower urinary tract

Abstract

Inflammation of the lower urinary tract occurs frequently in people. The causes remain obscure, with the exception of urinary tract infection. Animal models have proven useful for investigating and assessing mechanisms underlying symptoms associated with lower urinary tract inflammation and options for suppressing these symptoms. This review will discuss various animal models of lower urinary tract inflammation, including feline spontaneous (interstitial) cystitis, neurogenic cystitis, autoimmune cystitis, cystitis induced by intravesical instillation of chemicals or bacterial products (particularly lipopolysaccharide or LPS), and prostatic inflammation initiated by transurethral instillation of bacteria. Animal models will continue to be of significant value in identifying mechanisms resulting in bladder inflammation, but the relevance of some of these models to the causes underlying clinical disease is unclear. This is primarily because of the lack of understanding of causes of these disorders in people. Comparative and translational studies are required if the full potential of findings obtained with animal models to improve prevention and treatment of lower urinary tract inflammation in people is to be realized.

Figure 1

Four (A) and 24 hours (B) after instillation of acrolein (6, 10, or 100 μg; 15 μl total volume) or 15 μl phosphate buffered saline (PBS; control) into the bladders of female C57BL6N mice, it was observed that the severity of inflammation as indicated by intramural edema and hemorrhage correlated with increasing concentrations of acrolein. (L, lumen; D, detrusor); 40x original; scale bar = 200 μm. (With permission from: Bjorling DE, Elkahwaji JE, Bushman W, Janda LM, Boldon K, Hopkins WJ, Wang ZY. Acute acrolein-induced cystitis in mice. BJU Int 2007;99:1523-1529.)

Figure 1

Four (A) and 24 hours (B) after instillation of acrolein (6, 10, or 100 μg; 15 μl total volume) or 15 μl phosphate buffered saline (PBS; control) into the bladders of female C57BL6N mice, it was observed that the severity of inflammation as indicated by intramural edema and hemorrhage correlated with increasing concentrations of acrolein. (L, lumen; D, detrusor); 40x original; scale bar = 200 μm. (With permission from: Bjorling DE, Elkahwaji JE, Bushman W, Janda LM, Boldon K, Hopkins WJ, Wang ZY. Acute acrolein-induced cystitis in mice. BJU Int 2007;99:1523-1529.)

Figure 2

Prostatic inflammation was induced by a single transurethral instillation of E. coli 1677 in C3H/OuJ mice as previously described (141). A. Instillation of saline failed to cause any histological response when tissues from mice sacrificed 5 days after infusion were stained with hematoxylin and eosin. B. Five days after instillation of E. coli 1677, evidence of acute inflammation (AI) characterized by edema, inflammatory cell infiltrate, and exfoliation of epithelial cells into the ducts was observed. C. and D. Chronic inflammation (CI) consisting of dense accumulation of lymphocytes was present in the coagulating gland 12 weeks after instillation of bacteria, as well as evidence of early dysplastic changes in the ductal wall (D). 10x original. (With permission from: Elkahwaji JE, Zhong W, Hopkins WJ, Bushman W.Chronic bacterial infection and inflammation incite reactive hyperplasia in a mouse model of chronic prostatitis. Prostate 2007;67:14-21.)

Figure 2

Prostatic inflammation was induced by a single transurethral instillation of E. coli 1677 in C3H/OuJ mice as previously described (141). A. Instillation of saline failed to cause any histological response when tissues from mice sacrificed 5 days after infusion were stained with hematoxylin and eosin. B. Five days after instillation of E. coli 1677, evidence of acute inflammation (AI) characterized by edema, inflammatory cell infiltrate, and exfoliation of epithelial cells into the ducts was observed. C. and D. Chronic inflammation (CI) consisting of dense accumulation of lymphocytes was present in the coagulating gland 12 weeks after instillation of bacteria, as well as evidence of early dysplastic changes in the ductal wall (D). 10x original. (With permission from: Elkahwaji JE, Zhong W, Hopkins WJ, Bushman W.Chronic bacterial infection and inflammation incite reactive hyperplasia in a mouse model of chronic prostatitis. Prostate 2007;67:14-21.)

Figure 2

Prostatic inflammation was induced by a single transurethral instillation of E. coli 1677 in C3H/OuJ mice as previously described (141). A. Instillation of saline failed to cause any histological response when tissues from mice sacrificed 5 days after infusion were stained with hematoxylin and eosin. B. Five days after instillation of E. coli 1677, evidence of acute inflammation (AI) characterized by edema, inflammatory cell infiltrate, and exfoliation of epithelial cells into the ducts was observed. C. and D. Chronic inflammation (CI) consisting of dense accumulation of lymphocytes was present in the coagulating gland 12 weeks after instillation of bacteria, as well as evidence of early dysplastic changes in the ductal wall (D). 10x original. (With permission from: Elkahwaji JE, Zhong W, Hopkins WJ, Bushman W.Chronic bacterial infection and inflammation incite reactive hyperplasia in a mouse model of chronic prostatitis. Prostate 2007;67:14-21.)

Figure 2

Prostatic inflammation was induced by a single transurethral instillation of E. coli 1677 in C3H/OuJ mice as previously described (141). A. Instillation of saline failed to cause any histological response when tissues from mice sacrificed 5 days after infusion were stained with hematoxylin and eosin. B. Five days after instillation of E. coli 1677, evidence of acute inflammation (AI) characterized by edema, inflammatory cell infiltrate, and exfoliation of epithelial cells into the ducts was observed. C. and D. Chronic inflammation (CI) consisting of dense accumulation of lymphocytes was present in the coagulating gland 12 weeks after instillation of bacteria, as well as evidence of early dysplastic changes in the ductal wall (D). 10x original. (With permission from: Elkahwaji JE, Zhong W, Hopkins WJ, Bushman W.Chronic bacterial infection and inflammation incite reactive hyperplasia in a mouse model of chronic prostatitis. Prostate 2007;67:14-21.)