Allergen-induced depression of neutrophil chemotaxis in allergic individuals

In previous studies we have shown that neutrophil (PMN) chemotaxis is depressed in patients with allergic disease, hyperimmunoglobulinemia E, and recurrent infections. Although a number of these patients have now been described, little is known about the mechanism of defective PMN function in such individuals. The present studies were carried out to define the relationship between defective PMN chemotaxis and allergic hypersensitivity. Neutrophil chemotaxis was assessed in individuals with sensitivity to ragweed pollen as documented by intradermal skin testing. In each patient, chemotaxis was measured before and after in vitro exposure of their leukocytes to ragweed. A total of 21 individuals in 3 groups have been studied. These include 7 patients with allergic symptomatology and recurrent infections who were ragweed sensitive, 6 patients with a prior history of ragweed sensitivity who had undergone successful desensitization, and 8 nonatopic control subjects. Following in vitro exposure of the leukocytes of the 7 symptomatic patients to ragweed, a profound depression (54% ± 16%) in chemotatic activity was noted. In contrast the control subjects and 6 desensitized patients showed no depression of PMN chemotaxis. Further studies were carried out which demonstrate the antigen-specific nature of the phenomenon and the ability to transfer the depression to normal cells suspended in allergic serum. These data suggest that defective PMN chemotaxis in allergic patients results from an interaction, either directly or indirectly, of antigen with sensitized leukocytes. Specific immunotherapy may have an effect to prevent the chemotactic abnormality in these patients.