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Infection and Immunity, November 1999, p. 5820-5826, Vol. 67, No. 11
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Local Production of Chemokines during Experimental Vaginal Candidiasis

Michael Saavedra,1 Brad Taylor,1 Nicholas Lukacs,2 and Paul L. Fidel Jr.1,*

Department of Microbiology, Immunology, and Parasitology, Louisiana State University Medical Center, New Orleans, Louisiana,1 and Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan2

Received 17 May 1999/Returned for modification 28 June 1999/Accepted 2 September 1999

Recurrent vulvovaginal candidiasis, caused by Candida albicans, is a significant problem in women of childbearing age. Although cell-mediated immunity (CMI) due to T cells and cytokines is the predominant host defense mechanism against C. albicans at mucosal tissue sites, host defense mechanisms against C. albicans at the vaginal mucosa are poorly understood. Based on an estrogen-dependent murine model of vaginal candidiasis, our data suggest that systemic CMI is ineffective against C. albicans vaginal infections. Thus, we have postulated that local immune mechanisms are critical for protection against infection. In the present study, the kinetic production of chemokines normally associated with the chemotaxis of T cells, macrophages (RANTES, MIP-1alpha , MCP-1), and polymorphonuclear neutrophils (MIP-2) was examined following intravaginal inoculation of C. albicans in estrogen-treated or untreated mice. Results showed significant increases in MCP-1 protein and mRNA in vaginal tissue of infected mice as early as 2 and 4 days postinoculation, respectively, that continued through a 21-day observation period, irrespective of estrogen status. No significant changes were observed with RANTES, MIP-1alpha , or MIP-2, although relatively high constitutive levels of RANTES mRNA and MIP-2 protein were observed. Furthermore, intravaginal immunoneutralization of MCP-1 with anti-MCP-1 antibodies resulted in a significant increase in vaginal fungal burden early during infection, suggesting that MCP-1 plays some role in reducing the fungal burden during vaginal infection. However, the lack of changes in leukocyte profiles in vaginal lavage fluids collected from infected versus uninfected mice suggests that MCP-1 functions to control vaginal C. albicans titers in a manner independent of cellular chemotactic activity.

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

Infection and Immunity, November 1999, p. 5820-5826, Vol. 67, No. 11
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Nomanbhoy, F., Steele, C., Yano, J., Fidel, P. L. Jr. (2002). Vaginal and Oral Epithelial Cell Anti-Candida Activity. Infect. Immun. 70: 7081-7088 [Abstract] [Full Text]  
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