Department of Veterinary Parasitology, School of Veterinary Medicine, Kitasato University, Towada, Aomori, Japan.
Am J Trop Med Hyg. 2013 Feb;88(2):367-75. doi: 10.4269/ajtmh.2012.12-0338. Epub 2012 Dec 18.
Sex-based-differences are known to affect susceptibility to protozoan infections, but their effects on parasitemia and clinical symptoms in Babesia infections remain unclear. We examined the sex-based susceptibility of various mouse strains to Babesia microti Munich strain infection. In all strains, male mice exhibited significantly higher peak parasitemia and more severe anemia than female mice. Testosterone and estradiol-17β treatment caused an increase in parasitemia and aggravation of anemia. Orchidectomized male mice receiving testosterone exhibited smaller splenic macrophage populations three days after infection, smaller B cell populations 10 days after infection, and reduced splenic tumor necrosis factor-α and interferon-γ mRNA expression than mice that did not receive testosterone. Mice receiving estradiol-17β did not exhibit immunosuppressive effects. Thus, a weakened and delayed innate immunity response may lead to acquired immunity failure. The results suggested that testosterone directly affects T or B cells, leading to delayed acquired immunity, dramatically increased parasitemia, and severe anemia.
性别差异已知会影响对原生动物感染的易感性,但它们对巴贝虫感染中的寄生虫血症和临床症状的影响仍不清楚。我们检查了各种小鼠品系对微小巴贝斯虫慕尼黑株感染的性别易感性。在所有品系中,雄性小鼠的峰值寄生虫血症和贫血程度均显著高于雌性小鼠。睾酮和雌二醇-17β处理会导致寄生虫血症增加和贫血加重。接受睾酮治疗的去势雄性小鼠在感染后 3 天表现出较小的脾巨噬细胞群,在感染后 10 天表现出较小的 B 细胞群,并且脾肿瘤坏死因子-α和干扰素-γ mRNA 表达减少,而未接受睾酮治疗的小鼠则没有。接受雌二醇-17β的小鼠没有表现出免疫抑制作用。因此,较弱和延迟的先天免疫反应可能导致获得性免疫失败。结果表明,睾酮直接影响 T 或 B 细胞,导致获得性免疫延迟、寄生虫血症显著增加和严重贫血。