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Infection and Immunity, May 2004, p. 2939-2946, Vol. 72, No. 5
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.5.2939-2946.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

An Intravaginal Live Candida Challenge in Humans Leads to New Hypotheses for the Immunopathogenesis of Vulvovaginal Candidiasis

Paul L. Fidel Jr.,1* Melissa Barousse,1 Terri Espinosa,2 Mercedes Ficarra,1 Joy Sturtevant,1 David H. Martin,3 Alison J. Quayle,1 and Kathleen Dunlap2

Department of Microbiology, Immunology, and Parasitology,1 Department of Obstetrics and Gynecology,2 Section of Infectious Disease, Department of Medicine, Louisiana State University Health Sciences Center, New Orleans, Louisiana3

Received 15 October 2003/ Returned for modification 1 December 2003/ Accepted 30 January 2004

Acute and recurrent vulvovaginal candidiasis (VVC) remains a significant problem in women of childbearing age. While clinical studies of women with recurrent VVC (RVVC) and animal models have provided important data about a limited protective role of adaptive immunity, there remains a paucity of information on the protective mechanisms or factors associated with susceptibility to infection. In the present study, an intravaginal live Candida challenge in healthy adult women showed a differential susceptibility to symptomatic VVC, where 3 (15%) of 19 women with no history of VVC acquired a symptomatic infection compared to 6 (55%) of 11 women with an infrequent history of VVC. Furthermore, these studies revealed that protection against infection is noninflammatory while symptomatic infection correlates with a vaginal infiltration of polymorphonuclear neutrophils (PMNs) and a high vaginal fungal burden. Thus, the presence of symptomatic infection appears more dependent on host factors than on properties of the organism. Finally, vaginal lavage fluid from women with a symptomatic infection, but not those asymptomatically colonized, promoted the chemotaxis of PMNs. These results suggest that rather than RVVC/VVC being caused by an aberrant adaptive immune response, symptoms that define infection appear to be due to an aggressive innate response by PMNs.

* Corresponding author. Mailing address: Department of Microbiology, Immunology, and Parasitology, Louisiana State University Health Sciences Center, 1901 Perdido St., New Orleans, LA 70112. Phone and Fax: (504) 568-4066. E-mail: pfidel{at}lsuhsc.edu.

Editor: T. R. Kozel

Infection and Immunity, May 2004, p. 2939-2946, Vol. 72, No. 5
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.5.2939-2946.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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