Neisseria gonorrhoeae colonises the genital tract of oestradiol-treated germ-free female mice

Taylor‐Robinson, David; Furr, P. M.; Hetherington, C. M.

doi:10.1016/0882-4010(90)90071-w

Cited by 38 publications

(32 citation statements)

References 16 publications

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“…Of importance, single drug regimens were not sufficient for success, because estradiol, L. acidophilus , or antibiotics alone did not increase persistence, even though similar treatments were reported to increase susceptibility to murine vaginal infection with Mycoplasma hominis , Neisseria gonorrhoeae , or Ureaplasma urealyticum . [29][30][31] The combination of estradiol and L. acidophilus increased the rate and duration of murine T. vaginalis infection in some studies, 5,6 but this could not be reproduced, for unknown reasons, in our work or that of others. 7 Instead, we found that lowering vaginal PMNs by a combination of estradiol and dexamethasone was the best pretreatment strategy for obtaining persistent infection of mice with T. vaginalis .…”

Section: Discussioncontrasting

confidence: 40%

Murine Models of Vaginal Trichomonad Infections

Cobo¹,

Eckmann²,

Corbeil³

2011

The American Society of Tropical Medicine and Hygiene

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Abstract. Trichomonas vaginalis and Tritrichomonas foetus cause common sexually transmitted infections in humans and cattle, respectively. Mouse models of trichomoniasis are important for pathogenic and therapeutic studies. Here, we compared murine genital infections with T. vaginalis and T. foetus . Persistent vaginal infection with T. foetus was established with 100 parasites but T. vaginalis infection required doses of 10 6 , perhaps because of greater susceptibility to killing by mouse vaginal polymorphonuclear leukocytes. Infection with T. vaginalis persisted longest after combined treatment of mice with estrogen and dexamethasone, whereas infection was only short-lived when mice were given estrogen or dexamethasone alone, co-infected with Lactobacillus acidophilus , and/or pretreated with antibiotics. Infection rates were similar with metronidazole-resistant (MR) and metronidazole-sensitive (MS) T. vaginalis. High dose but not low dose metronidazole treatment controlled infection with MS better than MR T. vaginalis. These murine models will be valuable for investigating the pathogenesis and treatment of trichomoniasis.

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Section: Discussioncontrasting

confidence: 40%

Murine Models of Vaginal Trichomonad Infections

Cobo¹,

Eckmann²,

Corbeil³

2011

The American Society of Tropical Medicine and Hygiene

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“…Thus, it is possible that data obtained from primary cell and organ culture might provide only a small hint of gonococcal pathogenesis as it occurs in vivo at any site within the female genital tract. The development of a female mouse model of genital tract infection has served and will continue to serve as a valuable tool by which to study gonococcal pathogenesis in an immunologically defined environment (116,132,243). However, it is currently not clear whether data obtained from the mouse model of female genital tract infection is reflective of infection as it occurs within the human female genital tract, because mice fail to express several human-specific receptors (e.g., CR3, CD46, and CEACAM) that are believed to play critical roles in potentiating gonococcal disease.…”

Section: Models Used To Study Gonococcal Pathogenesismentioning

confidence: 99%

The Molecular Mechanisms Used byNeisseria gonorrhoeaeTo Initiate Infection Differ between Men and Women

2004

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The molecular mechanisms used by the gonococcus to initiate infection exhibit gender specificity. The clinical presentations of disease are also strikingly different upon comparison of gonococcal urethritis to gonococcal cervicitis. An intimate association occurs between the gonococcus and the urethral epithelium and is mediated by the asialoglycoprotein receptor. Gonococcal interaction with the urethral epithelia cell triggers cytokine release, which promotes neutrophil influx and an inflammatory response. Similarly, gonococcal infection of the upper female genital tract also results in inflammation. Gonococci invade the nonciliated epithelia, and the ciliated cells are subjected to the cytotoxic effects of tumor necrosis factor alpha induced by gonococcal peptidoglycan and lipooligosaccharide. In contrast, gonococcal infection of the lower female genital tract is typically asymptomatic. This is in part the result of the ability of the gonococcus to subvert the alternative pathway of complement present in the lower female genital tract. Gonococcal engagement of complement receptor 3 on the cervical epithelia results in membrane ruffling and does not promote inflammation. A model of gonococcal pathogenesis is presented in the context of the male and female human urogenital tracts

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“…Systemic regulation of sex hormones prior to vaginal inoculation affords several important advantages for experimental manipulation, including rendering otherwise-resistant animals susceptible to infection and arresting the reproductive cycle to synchronize the estrus phase of animals within a study (43). With regard to mycoplasmas, it is unclear why some species, such as M. pneumoniae and M. pulmonis, require progesterone treatment whereas others, including the genital pathogen M. fermentans, colonize the genital tract only following estrogen treatment (10).…”

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confidence: 99%

Mycoplasma genitalium Rapidly Disseminates to the Upper Reproductive Tracts and Knees of Female Mice following Vaginal Inoculation

2010

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Mycoplasma genitalium is an emerging sexually transmitted infection and in women isMycoplasma genitalium is an emerging sexually transmitted pathogen that was first identified as a cause of inflammatory urogenital disease in men (reviewed in references 15 and 18). Importantly, M. genitalium infections in women have also been associated with inflammatory syndromes, including cervicitis (8,24,27,32,50) and pelvic inflammatory disease (12), and (serologically) with impaired fertility (4, 37). Mechanistically, M. genitalium has previously been shown to activate highly expressed Toll-like receptors in reproductive tract epithelia, leading to inflammation (28,29). Collectively, these associations have led to an increased awareness of M. genitalium as a pathogen that could adversely affect reproductive health. It may also be of considerable importance that M. genitalium is strongly associated with HIV infections in men and women (reviewed in reference 31), suggesting that reproductive tract infections by M. genitalium may increase the likelihood of acquiring or transmitting other genital pathogens.Although the genital tract seems to be a preferred site of colonization, M. genitalium also has been a suspected cause of reactive arthritis, since DNA was previously detected in the knee joints of arthritic patients (45, 47) and in synovial fluid from temporomandibular joints (23). It is possible that M. genitalium may be a cause of sexually acquired reactive arthritis, but to date, no direct evidence exists for an association with an arthritic condition. Furthermore, no published reports have addressed the ability of M. genitalium to disseminate from the vagina to colonize the joint tissues or upper genital tract tissues. Similarly, there is a lack of experimental evidence for the causal associations of M. genitalium infection with inflammatory disease syndromes in women.As epidemiological data continue to implicate M. genitalium as a cause of reproductive tract disease, relevant animal models to investigate pathogenesis and evaluate therapeutic interventions are of utmost importance. Five years after the initial isolation of M. genitalium from men with urethritis (48), several large-animal species, including male cynomolgus monkeys (Macaca fascicularis), male chimpanzees (Pan troglodytes), female squirrel monkeys (Saimiri sciureus), female tamarins (Saguinus mystax), and female marmosets (Callithrix jacchus [44]), were found to be susceptible to experimental urogenital infection. These studies provided excellent preliminary evidence that M. genitalium could establish infection of female reproductive tract tissues. However, the cost of developing and maintaining primate and large-animal models prohibits experimentation employing larger-scale studies to address biological variability as part of an effective model of reproductive tract disease. In contrast, rodent models are cost-effective and afford the opportunity to investigate larger study populations of animals with specific genetic characteristics. Such models also allo...

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Neisseria gonorrhoeae colonises the genital tract of oestradiol-treated germ-free female mice

Cited by 38 publications

References 16 publications

Murine Models of Vaginal Trichomonad Infections

Murine Models of Vaginal Trichomonad Infections

The Molecular Mechanisms Used byNeisseria gonorrhoeaeTo Initiate Infection Differ between Men and Women

Mycoplasma genitalium Rapidly Disseminates to the Upper Reproductive Tracts and Knees of Female Mice following Vaginal Inoculation

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