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Keywords:

  • Candida infection;
  • oral mucosa;
  • oral immunity

In our experimental model of oral candiasis in the CD1 mouse, the primary infection showed reproducible Candida overgrowth kinetics with a peak level on day 5 of the infection. After day 7, the population stabilized at about 300 colony-forming units per excised mucosal tissue. The primary infection triggered an inflammatory response that resolved in under 8 days. At this point, the histological pattern of the mucosa reached a new equilibrium between recruited and resident mononuclear cells. The primary infection also rapidly stimulated cellular immunity, as measured from day 4 by a delayed-type hypersensitivity footpad reaction. Following a second topical challenge with Candida 30 days after the primary infection, the infection was barely delectable and a typical local delayed-type hypersensitivity reaction occurred between 24–72 h. It is proposed that acquired resistance, in conjunction with low-level persistence of Candida in our model, mimics the carrier stale in sensitized humans.