BACKGROUND Chronic prostatitis has been supposed to be associated with preneoplastic lesions and cancer development. The objective of this study was to examine how chronic inflammation results in a prostatic microenvironment and gene mutation in C57BL/6 mice. METHODS Immune and bacterial prostatitis mouse models were created through abdominal subcutaneous injection of rat prostate extract protein immunization (EAP group) or transurethral instillation of uropathogenic E. coli 1677 (E. coli group). Prostate histology, serum cytokine level, and genome-wide exome (GWE) sequences were examined 1, 3, and 6 months after immunization or injection. RESULT In the EAP and E. coli groups, immune cell infiltrations were observed in the first and last months of the entire experiment. After 3 months, obvious proliferative inflammatory atrophy (PIA) and prostatic intraepithelial neoplasia (PIN) were observed accompanied with fibrosis hyperplasia in stroma. The decrease in basal cells (Cytokeratin (CK) 5+/p63+) and the accumulation of luminal epithelial cells (CK8+) in the PIA or PIN area indicated that the basal cells were damaged or transformed into different luminal cells. Hic1, Zfp148, and Mfge8 gene mutations were detected in chronic prostatitis somatic cells. CONCLUSION Chronic prostatitis induced by prostate extract protein immunization or E. coli infection caused a reactive prostatic inflammation microenvironment and resulted in tissue damage, aberrant atrophy, hyperplasia, and somatic genome mutation.

中文翻译：

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慢性前列腺炎会改变C57BL / 6小鼠的前列腺微环境并加速肿瘤前病变。

背景技术据信慢性前列腺炎与肿瘤前病变和癌症发展有关。这项研究的目的是检查慢性炎症如何导致C57BL / 6小鼠的前列腺微环境和基因突变。方法通过腹部皮下注射大鼠前列腺提取物蛋白免疫疫苗（EAP组）或经尿道灌输尿路致病性大肠杆菌1677（大肠杆菌组），建立免疫和细菌性前列腺炎小鼠模型。免疫或注射后1、3和6个月检查前列腺组织学，血清细胞因子水平和全基因组外显子组（GWE）序列。结果在EAP和E. coli组中，在整个实验的前几个月和最后几个月观察到免疫细胞浸润。3个月后，在基质中观察到明显的增生性炎症性萎缩（PIA）和前列腺上皮内瘤变（PIN）并伴有纤维化增生。PIA或PIN区域中基底细胞（Cytokeratin（CK）5 + / p63 +）的减少和腔上皮细胞（CK8 +）的积累表明，基底细胞受损或转化为不同的腔细胞。在慢性前列腺炎的体细胞中检测到Hic1，Zfp148和Mfge8基因突变。结论前列腺提取物蛋白免疫或大肠杆菌感染引起的慢性前列腺炎引起反应性前列腺炎症微环境，并导致组织损伤，异常萎缩，增生和体细胞基因组突变。PIA或PIN区域中基底细胞（Cytokeratin（CK）5 + / p63 +）的减少和腔上皮细胞（CK8 +）的积累表明，基底细胞受损或转化为不同的腔细胞。在慢性前列腺炎的体细胞中检测到Hic1，Zfp148和Mfge8基因突变。结论前列腺提取物蛋白免疫或大肠杆菌感染引起的慢性前列腺炎引起反应性前列腺炎症微环境，并导致组织损伤，异常萎缩，增生和体细胞基因组突变。PIA或PIN区域中基底细胞（Cytokeratin（CK）5 + / p63 +）的减少和腔上皮细胞（CK8 +）的积累表明，基底细胞受损或转化为不同的腔细胞。在慢性前列腺炎的体细胞中检测到Hic1，Zfp148和Mfge8基因突变。结论前列腺提取物蛋白免疫或大肠杆菌感染引起的慢性前列腺炎引起反应性前列腺炎症微环境，并导致组织损伤，异常萎缩，增生和体细胞基因组突变。