Mouse model for acute bacterial prostatitis in genetically distinct inbred strains

Mouse model for acute bacterial prostatitis in genetically distinct inbred strains
复制标题

DOI:
10.1016/j.urology.2005.04.013
复制
发表时间:
2005-10-01
期刊:
影响因子:
2.1
通讯作者:
Hopkins, WJ
Hopkins, WJ
中科院分区:
医学4区
文献类型:
--
作者:
Elkahwaji, JE;Ott, CJ;Hopkins, WJ

文献摘要

被引文献

相似文献

目标.前列腺炎是一种常见于成年男性的泌尿系统疾病。多达50%的男性在其一生中会经历一次前列腺炎发作,并且2%至3%的男性会患有细菌性前列腺炎。由于前列腺炎的致病机制尚不清楚,我们开发了一种可重复的细菌性前列腺炎小鼠模型,以研究与感染易感性相关的病原学和宿主因素。13周龄雄性BALB/c、C3 H/HeJ、C3 H/HeOuJ、C57 BL/6 J和(BALB/c x C3 H/HeJ)F小鼠经尿道内接种2 x 10(6)或2 x 10(8)大肠埃希菌。对照小鼠接种磷酸盐缓冲盐水。接种后第5天处死动物,以评估膀胱和前列腺感染的强度。在任一接种物剂量下,BALB/c、C57/BL/6 J或(BALB/c x C3 H/HeJ)F小鼠中均不存在显著的膀胱或前列腺感染。相比之下,C3 H/HeJ和C3 H/HeOuJ小鼠在两种剂量下都发生了高膀胱感染和严重的急性前列腺炎。用磷酸盐缓冲盐水感染的对照小鼠没有膀胱或前列腺感染。C3 H/HeJ或C3 H/HeOuJ与BALB/c、C57 BL/6 J或F-1小鼠膀胱和前列腺集落形成单位的比较P值均小于0.01。敏感性的菌株依赖性差异表明遗传因素可能在细菌性前列腺炎的病因学中起主要作用。因为F-1小鼠没有发生显著的膀胱和前列腺感染,与BALB/c亲本相似,所以感染易感性似乎是一种隐性性状。该模型的可用性将使我们能够研究细菌的免疫学、遗传学和组织病理学特征。前列腺感染
Objectives. Prostatitis is a common urologic disease seen in adult men. As many as 50% of men will experience an episode of prostatitis in their lifetime, and 2% to 3% of men will have bacterial prostatitis Because the pathogenic mechanisms of prostatitis remain unclear, we developed a reproducible mouse model of bacterial prostatitis in which to study the etiology and host factors associated with infection susceptibility.Methods. Male BALB/c, C3H/HeJ, C3H/HeOuJ, C57BL/6J, and (BALB/c x C3H/HeJ)F, mice 13 weeks old were inoculated intraurethrally with 2 x 10(6) or 2 x 10(8) Escherichia coli. Control mice were inoculated with phosphate-buffered saline. The animals were killed at 5 days after inoculation to assess the intensities of the bladder and prostate infections.Results. Significant bladder or prostate infections were not present in the BALB/c, C57/BL/6J, or (BALB/c x C3H/HeJ)F, mice at either inoculum dose. In contrast, both C3H/HeJ and C3H/HeOuJ mice developed high bladder infections and severe, acute prostatitis at both doses. Control mice infected with phosphate-buffered saline had no bladder or prostate infections. The P values were less than 0.01 for the comparison of bladder and prostate colony-forming units between C3H/HeJ or C3H/HeOuJ and BALB/c, C57BL/6J, or F-1 mice.Conclusions. The strain-dependent differences in susceptibility indicate that genetic factors may play a major role in the etiology of bacterial prostatitis. Because F-1 mice did not develop significant bladder and prostate infections, similar to the BALB/c parents, it appears that infection-susceptibility is a recessive trait. The availability of this model will allow us to investigate the immunology, genetics, and histopathologic features of bacterial. infection of the prostate.