Khosravi Farhad, Michel Vera, Galuska Christina E, Bhushan Sudhanshu, Christian Philipp, Schuppe Hans-Christian, Pilatz Adrian, Galuska Sebastian P, Meinhardt Andreas
From the Institutes of Anatomy and Cell Biology and Biochemistry and.
From the Institutes of Anatomy and Cell Biology and.
J Biol Chem. 2016 Aug 19;291(34):17717-26. doi: 10.1074/jbc.M116.718072. Epub 2016 Jun 23.
Urinary tract infections caused by uropathogenic Escherichia coli (UPEC) pathovars belong to the most frequent infections in humans. In men, pathogens can also spread to the genital tract via the continuous ductal system, eliciting bacterial prostatitis and/or epididymo-orchitis. Antibiotic treatment usually clears pathogens in acute epididymitis; however, the fertility of patients can be permanently impaired. Because a premature acrosome reaction was observed in an UPEC epididymitis mouse model, and sialidases on the sperm surface are considered to be activated via proteases of the acrosome, we aimed to investigate whether alterations of the sialome of epididymal spermatozoa and surrounding epithelial cells occur during UPEC infection. In UPEC-elicited acute epididymitis in mice, a substantial loss of N-acetylneuraminic acid residues was detected in epididymal spermatozoa and epithelial cells using combined laser microdissection/HPLC-ESI-MS analysis. In support, a substantial reduction of sialic acid residues bound to the surface of spermatozoa was documented in men with a recent history of E. coli-associated epididymitis. In vitro, such an UPEC induced N-acetylneuraminic acid release from human spermatozoa was effectively counteracted by a sialidase inhibitor. These findings strongly suggest a substantial remodeling of the glycocalyx of spermatozoa and epididymal epithelial cells by endogenous sialidases after a premature acrosome reaction during acute epididymitis.
由尿路致病性大肠杆菌(UPEC)致病型引起的尿路感染是人类最常见的感染之一。在男性中,病原体还可通过连续的管道系统扩散至生殖道,引发细菌性前列腺炎和/或附睾睾丸炎。抗生素治疗通常可清除急性附睾炎中的病原体;然而,患者的生育能力可能会受到永久性损害。由于在UPEC附睾炎小鼠模型中观察到顶体过早反应,并且精子表面的唾液酸酶被认为是通过顶体蛋白酶激活的,因此我们旨在研究在UPEC感染期间附睾精子和周围上皮细胞的唾液酸组是否发生改变。在小鼠由UPEC引发的急性附睾炎中,使用激光显微切割/HPLC-ESI-MS联用分析检测到附睾精子和上皮细胞中N-乙酰神经氨酸残基大量缺失。同样,近期有大肠杆菌相关性附睾炎病史的男性中,精子表面结合的唾液酸残基也大幅减少。在体外,唾液酸酶抑制剂可有效抑制UPEC诱导的人精子N-乙酰神经氨酸释放。这些发现有力地表明,急性附睾炎期间顶体过早反应后,内源性唾液酸酶会使精子和附睾上皮细胞的糖萼发生显著重塑。