Protective host defense mechanisms against vaginal Candida albicans
infections are poorly understood. Although cell-mediated immunity (CMI) is the predominant host defense mechanism against most mucosal
Candida infections, the role of CMI against vaginal
candidiasis is uncertain, both in humans and in an experimental mouse model. The role of humoral immunity is equally unclear. While clinical observations suggest a minimal role for
antibodies against vaginal
candidiasis, an experimental rat model has provided evidence for a protective role for Candida-specific
immunoglobulin A (
IgA)
antibodies. Additionally, Candida vaccination-induced
IgM and
IgG3 antibodies are protective in a mouse model of
vaginitis. In the present study, the role of
infection-induced humoral immunity in protection against experimental vaginal
candidiasis was evaluated through the quantification of Candida-specific
IgA,
IgG, and
IgM antibodies in serum and vaginal lavage fluids of mice with primary and secondary (partially protected)
infection. In naïve mice, total, but not Candida-specific,
antibodies were detected in serum and lavage fluids, consistent with lack of yeast colonization in mice. In infected mice, Candida-specific
IgA and
IgG antibodies were induced in serum with anamnestic responses to
secondary infection. In lavage fluid, while Candida-specific
antibodies were detectable, concentrations were extremely low with no anamnestic responses in mice with
secondary infection. The incorporation of alternative protocols-including
infections in a different strain of mice, prolongation of primary
infection prior to secondary challenge, use of different
enzyme-linked
immunosorbent assay capture
antigens, and concentration of lavage fluid-did not enhance local Candida-specific antibody production or detection. Additionally,
antibodies were not removed from lavage fluids by being bound to Candida during
infection. Together, these data suggest that
antibodies are not readily present in vaginal secretions of infected mice and thus have a limited natural protective role against
infection.