Urinary tract infections (UTIs) are generally considered a disease of women. However, UTIs affect females throughout the lifespan, and certain male populations (including infants and elderly men) are also susceptible. Epidemiologically, pyelonephritis is more common in women but carries increased morbidity when it does occur in men. Among children, high-grade vesicoureteral reflux is a primary risk factor for upper-tract UTI in both sexes. However, among young infants with UTI, girls are outnumbered by boys; risk factors include posterior urethral valves and lack of circumcision. Recent advances in mouse models of UTI reveal sex differences in innate responses to UTI, which vary somewhat depending on the system used. Moreover, male mice and androgenized female mice suffer worse outcomes in experimental pyelonephritis; evidence suggests that androgen exposure may suppress innate control of infection in the urinary tract, but additional androgen effects, as well as non-hormonal sex effects, may yet be specified. Among other intriguing directions, recent experiments raise the hypothesis that the postnatal testosterone surge that occurs in male infants may represent an additional factor driving the higher incidence of UTI in males under 6 months of age. Ongoing work in contemporary models will further illuminate sex- and sex-hormone-specific effects on UTI pathogenesis and immune responses.

中文翻译：

---

肾盂肾炎的性别影响。

尿路感染 (UTI) 通常被认为是一种女性疾病。然而，尿路感染会影响女性的整个生命周期，某些男性人群（包括婴儿和老年男性）也易感。流行病学上，肾盂肾炎在女性中更为常见，但在男性中确实发生时会增加发病率。在儿童中，高级别膀胱输尿管反流是男女上尿路感染的主要危险因素。然而，在患有尿路感染的小婴儿中，女孩的人数多于男孩；危险因素包括后尿道瓣膜和缺乏包皮环切术。UTI 小鼠模型的最新进展揭示了对 UTI 的先天反应的性别差异，这取决于所使用的系统而有所不同。此外，雄性小鼠和雄激素化的雌性小鼠在实验性肾盂肾炎中的结果更差；有证据表明，雄激素暴露可能会抑制对泌尿道感染的先天控制，但可能还需要说明额外的雄激素作用以及非激素性作用。在其他有趣的方向中，最近的实验提出了一个假设，即发生在男婴中的产后睾酮激增可能是推动 6 个月以下男性尿路感染发病率升高的另一个因素。当代模型中正在进行的工作将进一步阐明性激素和性激素对 UTI 发病机制和免疫反应的特异性影响。最近的实验提出了一个假设，即男婴中发生的产后睾酮激增可能是导致 6 个月以下男性尿路感染发病率升高的另一个因素。当代模型中正在进行的工作将进一步阐明性激素和性激素对 UTI 发病机制和免疫反应的特异性影响。最近的实验提出了一个假设，即男婴中发生的产后睾酮激增可能是导致 6 个月以下男性尿路感染发病率升高的另一个因素。当代模型中正在进行的工作将进一步阐明性激素和性激素对 UTI 发病机制和免疫反应的特异性影响。