title: Chlamydial induction of hydrosalpinx in 11 strains of mice reveals multiple host mechanisms for preventing upper genital tract pathology.
abstract: 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.
authors.affiliation: 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.
authors.forename: Jianlin
authors.initials: J
authors.lastname: Chen
authors.affiliation: 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.
authors.forename: Hongbo
authors.initials: H
authors.lastname: Zhang
authors.affiliation: Department of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
authors.forename: Zhou
authors.initials: Z
authors.lastname: Zhou
authors.affiliation: Department of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
authors.forename: Zhangsheng
authors.initials: Z
authors.lastname: Yang
authors.affiliation: Departments of Obstetrics and Gynecology, Pathology and Endocrinology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
authors.forename: Yiling
authors.initials: Y
authors.lastname: Ding
authors.affiliation: Departments of Obstetrics and Gynecology, Pathology and Endocrinology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
authors.forename: Zhiguang
authors.initials: Z
authors.lastname: Zhou
authors.affiliation: Department of Economics, University of Wisconsin-Madison, Madison, Wisconsin, United States of America.
authors.forename: Edward
authors.initials: E
authors.lastname: Zhong
authors.affiliation: Department of Biology, University of Texas at San Antonio, San Antonio, Texas, United States of America.
authors.forename: Bernard
authors.initials: B
authors.lastname: Arulanandam
authors.affiliation: Department of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
authors.forename: Joel
authors.initials: J
authors.lastname: Baseman
authors.affiliation: Department of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America.
authors.forename: Guangming
authors.initials: G
authors.lastname: Zhong
mesh_terms: D000818:Animals; D002690:Chlamydia Infections / Q000382:microbiology*; D023502:Chlamydia muridarum; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D006183:H-2 Antigens / Q000235:genetics; D006239:Haplotypes; D054884:Host-Pathogen Interactions; D051379:Mice; D060737:Reproductive Tract Infections / Q000235:genetics / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology*
chemical_list: D016207:Cytokines; D006183:H-2 Antigens
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