Study of possible mechanisms of basophil accumulation in experimental cutaneous candidiasis in guinea pigs.

It is known that certain lymphokine preparations, bacterial growth products, and factors released through complement activation have in vitro chemotactic activity for basophils. We have developed a model for acute cutaneous candidiasis in guinea pigs in which the lesions are characterized by infecting organisms in the keratin layer, early accumulation of polymorphonuclear leukocytes in the upper epidermis, and subsequent accumulation of basophils along the dermal basement membrane. The present study was undertaken to determine if any of the known chemotactic factors were operating in vivo to attract basophils. Both nonimmune guinea pigs and animals with established delayed hypersensitivity to candida had basophils in the infected skin. While immune animals showed more basophils than did nonimmune animals, the difference was not significant. Intradermal injections of a sonicate of candida or a candida growth filtrate did not cause significant accumulation of basophils. Decomplementation of the animals with cobra venom factor (CVF) did not significantly reduce the basophil numbers. Moreover, basophil accumulation occurred in animals with only minimal serum antibody to candida. These studies indicate that the basophil accumulation is due to a mechanism that is not dependent on cellular immunity, direct chemotactic activity in the candida extract, antibodies, or complement. Therefore, there may exist a previously unrecognized, nonimmunologic mechanism of chemotaxis for basophils which could possibly operate in other types of lesions and could even be involved with attraction of other types of cells.