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Epidermal proliferation in the defense against experimental cutaneous candidiasis.

In previous studies we implicated scaling of the stratum corneum as being important in the clearance of experimental cutaneous Candida infections in guinea pigs. In this model the scaling response appeared to be intensified by delayed hypersensitivity reactions to Candida antigens and to be responsible for the more rapid clearance of infecting organisms by immune animals. The present studies were undertaken to quantitate the degree of epidermal proliferation in such Candida infections and to relate it to delayed hypersensitivity reactions as well as other types of inflammation. The two parameters of epidermal proliferation studied were incorporation of tritiated thymidine by basal cells and thickening of the malpighian layer; both were increased markedly in Candida -infected skin of immune animals and also to a lesser extent in Candida -infected skin of nonimmune animals. Positive delayed skin test responses to Candida antigens were associated with increased basal cell thymidine incorporation, but negative delayed responses were not. Inflammation caused by intradermal injection of irritants was also associated with increased basal cell thymidine incorporation. These results indicate that delayed hypersensitivity reactions in experimental cutaneous Candida infections act to increase the rate of basal cell turnover, primarily by producing increased inflammation in the lesions. The role of delayed hypersensitivity appears to be nonspecific, since other forms of inflammation are also capable of causing increased epidermal proliferation.