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Infection and Immunity, November 2001, p. 7091-7099, Vol. 69, No. 11
Department of Microbiology, Immunology, and
Parasitology, Louisiana State University Health Sciences Center,
New Orleans, Louisiana 70112,1 and
Department of General Dentistry, Louisiana State University
School of Dentistry, New Orleans, Louisiana
701192
Received 11 May 2001/Returned for modification 9 July 2001/Accepted 8 August 2001
Candida albicans is both a commensal and a pathogen
at the oral mucosa. Although an intricate network of host defense
mechanisms are expected for protection against oropharyngeal
candidiasis, anti-Candida host defense mechanisms at the
oral mucosa are poorly understood. Our laboratory recently showed that
primary epithelial cells from human oral mucosa, as well as an oral
epithelial cell line, inhibit the growth of blastoconidia and/or hyphal
phases of several Candida species in vitro with a
requirement for cell contact and with no demonstrable role for soluble
factors. In the present study, we show that oral epithelial
cell-mediated anti-Candida activity is resistant to
gamma-irradiation and is not mediated by phagocytosis, nitric oxide,
hydrogen peroxide, and superoxide oxidative inhibitory pathways or by
nonoxidative components such as soluble defensin and calprotectin
peptides. In contrast, epithelial cell-mediated
anti-Candida activity was sensitive to heat,
paraformaldehyde fixation, and detergents, but these treatments were
accompanied by a significant loss in epithelial cell viability.
Treatments that removed existing membrane protein or lipid moieties in
the presence or absence of protein synthesis inhibitors had no effect
on epithelial cell inhibitory activity. In contrast, the epithelial
cell-mediated anti-Candida activity was abrogated after
treatment of the epithelial cells with periodic acid, suggesting a role
for carbohydrates. Adherence of C. albicans to oral
epithelial cells was unaffected, indicating that the carbohydrate
moiety is exclusively associated with the growth inhibition activity.
Subsequent studies that evaluated specific membrane carbohydrate
moieties, however, showed no role for sulfated polysaccharides, sialic
acid residues, or glucose- and mannose-containing carbohydrates. These
results suggest that oral epithelial cell-mediated
anti-Candida activity occurs exclusively with viable
epithelial cells through contact with C. albicans by an
as-yet-undefined carbohydrate moiety.
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.11.7091-7099.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Potential Role for a Carbohydrate Moiety in
Anti-Candida Activity of Human Oral Epithelial
Cells
*
Corresponding author. Mailing address: Department of
Microbiology, Immunology, and Parasitology, Louisiana State University Health Sciences Center, 1901 Perdido St., New Orleans, LA 70112. Phone: (504) 568-4066. Fax: (504) 568-4066. E-mail:
pfidel{at}lsuhsc.edu.
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