IAI Accepts, published online ahead of print on 9 November 2009

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Infect. Immun. doi:10.1128/IAI.00711-09
Copyright (c) 2009, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Mouse Strain-dependent Differences in Susceptibility to Neisseria gonorrhoeae Infection and Induction of Innate Immune Responses

Mathanraj Packiam, Sandra J Veit, Deborah J. Anderson, Robin R Ingalls^*, and Ann E Jerse^*

Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814; Department of Obstetrics and Gynecology, and Section of Infections Diseases, Boston University School of Medicine, Boston, MA 02118

^* To whom correspondence should be addressed. Email: ringalls{at}bu.edu. ajerse{at}usuhs.mil.

Acute gonorrhea in women is characterized by a mucopurulent exudate that contains polymorphonuclear leukocytes (PMNs) with intracellular gonococci. Asymptomatic infections are also common. Information on the innate response to Neisseria gonorrhoeae in women is limited to studies with cultured cells, isolated immune cells and analyses of cervicovaginal fluids. 17-estradiol-treated BALB/c mice can be experimentally infected with N. gonorrhoeae, and a vaginal PMN influx occurs in 50-80% of mice. Here we compared the colonization load and proinflammatory response of BALB/c, C57BL/6 and C3H/HeN mice to N. gonorrhoeae. BALB/c and C57BL/6 mice were colonized at similar levels following inoculation with 10⁶ colony forming units of N. gonorrhoeae. BALB/c, but not C57BL/6 mice exhibited a marked vaginal PMN influx. Tumor necrosis factor-alpha (TNF), interleukin-6 (IL-6), macrophage inflammatory protein 2 (MIP-2), and keratinocyte-derived chemokine (KC) were elevated in vaginal secretions from infected BALB/c mice but not C57BL/6 mice. MIP-2 levels positively correlated with a vaginal PMN influx. In contrast to BALB/c and C57BL/6 mice, C3H/HeN mice were resistant to infection and there was no evidence of an inflammatory response. We conclude N. gonorrhoeae causes a productive infection in BALB/c mice that is characterized by the induction of proinflammatory cytokines and chemokines and the recruitment of PMNs. Infection of C57/BL6 mice, in contrast, is more similar to asymptomatic infection. C3H/HeN mice are inherently resistant to N. gonorrhoeae infection, and this resistance is not due to an overwhelming inflammatory response to infection. Host genetic factors can therefore impact susceptibility and the immune response to N. gonorrhoeae.