ABSTRACT
Models of allergen challenge of the skin, the nose, or the lungs have revealed that such responses consist of an initial triggering of mediator-containing cells, followed by a succession of events beginning with the release of vasoactive, chemotactic, and spasmogenic mediators and followed by a delayed influx of inflammatory cells into the site of tissue damage. Vasoactive and spasmogenic mediators lead to the early-phase reaction, whereas cellular inflammatory influx is believed to be concomitant with the late-phase reaction. The chemotactic response of human isolated eosinophils can be induced using different chemotactic mediators. The pharmacological modulation of this response was assessed using this model. The skin is obviously easier to investigate in humans than the nose or the lungs. Usually the cutaneous cellular infiltration can be evaluated either by the technique of the Rebuck window, which is easy to perform, or by histology of a skin biopsy, which is much more invasive.
