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. 2006 Apr;74(4):2382-91.
doi: 10.1128/IAI.74.4.2382-2391.2006.

CD8+ T cells but not polymorphonuclear leukocytes are required to limit chronic oral carriage of Candida albicans in transgenic mice expressing human immunodeficiency virus type 1

Miriam Marquis  1 , Daniel Lewandowski, Véronique Dugas, Francine Aumont, Serge Sénéchal, Paul Jolicoeur, Zaher Hanna, Louis de Repentigny
Affiliations

CD8+ T cells but not polymorphonuclear leukocytes are required to limit chronic oral carriage of Candida albicans in transgenic mice expressing human immunodeficiency virus type 1

Miriam Marquis et al. Infect Immun. 2006 Apr.

Abstract

Candida albicans causes oropharyngeal candidiasis (OPC) but rarely disseminates to deep organs in human immunodeficiency virus (HIV) infection. Here, we used a model of OPC in CD4C/HIV(Mut) transgenic (Tg) mice to investigate the role of polymorphonuclear leukocytes (PMNs) and CD8+ T cells in limiting candidiasis to the mucosa. Numbers of circulating PMNs and their oxidative burst were both augmented in CD4C/HIV(MutA) Tg mice expressing rev, env, and nef of HIV type 1 (HIV-1), while phagocytosis and killing of C. albicans were largely unimpaired compared to those in non-Tg mice. Depletion of PMNs in these Tg mice did not alter oral or gastrointestinal burdens of C. albicans or cause systemic dissemination. However, oral burdens of C. albicans were increased in CD4C/HIV(MutG) Tg mice expressing only the nef gene of HIV-1 and bred on a CD8 gene-deficient background (CD8-/-), compared to control or heterozygous CD8+/- CD4C/HIV(MutG) Tg mice. Thus, CD8+ T cells contribute to the host defense against oral candidiasis in vivo, specifically in the context of nef expression in a subset of immune cells.

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Figures

FIG. 1.
FIG. 1.
Quantitation of peripheral blood leukocytes in CD4C/HIVMutA Tg and non-Tg mice infected with C. albicans or uninfected. Blood samples were drawn from Tg and non-Tg mice at 7 (A), 45 (B), or 70 (C) days after oral infection with C. albicans or from uninfected control animals. There were four to six mice per determination. Statistically significant differences between groups: *, P < 0.05 compared to infected or uninfected non-Tg mice; **, P < 0.05 compared to uninfected non-Tg mice; ***, P < 0.01 compared to uninfected non-Tg mice; ****, P < 0.05 compared to uninfected Tg or non-Tg mice; *****, P < 0.001 compared to infected non-Tg mice.
FIG. 2.
FIG. 2.
Oxidative burst of PMNs from CD4C/HIVMutA Tg and non-Tg mice infected with C. albicans or uninfected. Blood samples were drawn from Tg and non-Tg mice at 7 or 70 days after oral infection with C. albicans or from uninfected control animals. Data represent the means ± SDs from four independent observations, each obtained by pooling the blood of two mice. *, significantly different from uninfected non-Tg mice (P < 0.05).
FIG. 3.
FIG. 3.
Phagocytosis and killing of C. albicans blastoconidia by PMNs from CD4C/HIVMutA Tg and non-Tg mice infected with C. albicans or uninfected. Blood samples were obtained from Tg or non-Tg mice at 7 or 70 days after oral infection with C. albicans or from uninfected control animals. Analysis was performed at the indicated PMN/blastoconidia ratios. Data represent the means ± SDs from three to nine independent observations, each obtained by pooling the blood of 4 to 10 mice. *, P < 0.05 compared to non-Tg mice.
FIG. 4.
FIG. 4.
Oral burdens of C. albicans and absolute circulating PMNs in CD4C/HIVMutA Tg mice treated with RB6-8C5 monoclonal antibody (red lines) or isotype control (blue lines). Control non-Tg mice (green lines) were treated with RB6-8C5 monoclonal activity. Beginning on day 20 (A), 45 (B), or 63 (C) after oral infection with C. albicans, each group of mice received its respective treatment every 2 days until euthanasia 7 days later. Data represent the means ± SDs for six or seven mice in each group.
FIG. 5.
FIG. 5.
CD4C/HIVMutGCD8−/− Tg mice (red line), CD8−/− non-Tg mice (green line), CD4C/HIVMutG Tg mice (blue line), and non-Tg littermates (orange line) were infected intraorally with 108 CFU of C. albicans, and burdens were assessed longitudinally by sampling the oral cavity. Data represent the means ± SDs for 6, 6, 10, and 14 mice in each of these four groups, respectively.
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