Department of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America; Departments of Obstetrics and Gynecology, Pathology and Endocrinology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Department of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
PLoS One. 2014 Apr 15;9(4):e95076. doi: 10.1371/journal.pone.0095076. eCollection 2014.
The female lower genital tract is constantly exposed to microbial infection, some of which can ascend to and cause pathology such as hydrosalpinx in the upper genital tract, which can affect fertility. To understand host mechanisms for preventing upper genital tract pathology, we screened 11 inbred strains of mice for hydrosalpinx induction by C. muridarum. When examined on days 60 to 80 after intravaginal infection, the 11 strains fell into 3 groups based on their hydrosalpinx severity: CBA/J and SJL/J mice were highly susceptible with a hydrosalpinx score of 5 or greater; Balb/c, C57BL/6J, C57BL/10J, C3H/HeJ and C3H/HeN were susceptible with a score between 1 and <5; NOD/ShiLtJ, DBA/1J, DBA/2J and A/J were resistant with a score of <1. The diverse range of mouse susceptibility to hydrosalpinx induction may reflect the varied clinical outcomes of C. trachomatis-infected women. When the 11 strains were infected via an intrauterine inoculation to bypass the requirement for ascension, higher incidence and more severe hydrosalpinges were induced in most mice, indicating that the interaction between chlamydial ascension and host control of ascension is critical for determining susceptibility to hydrosalpinx development in many mice. However, a few mouse strains resisted significant exacerbation of hydrosalpinx by intrauterine infection, indicating that these mice have evolved ascension-independent mechanisms for preventing upper genital tract pathology. Together, the above observations have demonstrated that different strains of mice can prevent upper genital tract pathology by using different mechanisms.
女性下生殖道不断受到微生物感染的影响，其中一些感染可能会向上蔓延并导致输卵管积水等上生殖道疾病，从而影响生育能力。为了了解宿主预防上生殖道疾病的机制，我们筛选了 11 种近交系小鼠对 C. muridarum 引起的输卵管积水的易感性。在阴道感染后 60 至 80 天检查时，根据输卵管积水严重程度，这 11 种品系分为 3 组：CBA/J 和 SJL/J 小鼠高度易感，输卵管积水评分为 5 或更高；Balb/c、C57BL/6J、C57BL/10J、C3H/HeJ 和 C3H/HeN 易感，评分为 1 至 <5；NOD/ShiLtJ、DBA/1J、DBA/2J 和 A/J 具有抗性，评分为 <1。小鼠对输卵管积水诱导的易感性差异可能反映了沙眼衣原体感染妇女的不同临床结局。当 11 种品系通过宫内接种感染以绕过上升要求时，大多数小鼠的感染发生率更高，输卵管积水更严重，表明沙眼衣原体上升和宿主对上升的控制之间的相互作用对于确定许多小鼠输卵管积水发展的易感性至关重要。然而，少数小鼠品系对宫内感染引起的输卵管积水加重有明显抵抗力，表明这些小鼠已经进化出了不依赖上升的预防上生殖道疾病的机制。总之，上述观察结果表明，不同品系的小鼠可以通过不同的机制预防上生殖道疾病。
