DEFECTIVE NEUTROPHIL CHEMOTAXIS, SEVERE STAPHYLOCOCCAL INFECTION AND HYPERMMUNOGLOBULINEMIA E

Abstract

Neutrophil granulocyte function was determined in three patients with severe staphylococcal infection, clinical manifestations of allergic disease, and hyperimmunoglobulinemia E. Each of the patients had urticarial skin rashes before or at the time of development of staphylococcal suppurative lymphadenitis, pneumonia or sepsis. Neutrophil chemotaxis, random migration, phagocytosis and bactericidal capacity were assessed to determine if an abnormality in these functions might have contributed to the development of severe staphylococcal infection. Each of the 3 patients with increased IgE was found to have a marked defect in neutrophil chemotaxis. The mean chemotactic index of the patients was 12±4 while that of 20 controls was 72±17. Neutrophil random migration, phagocytosis and bactericidal capacity were normal in each patient. We have shown in previous studies that patients with eczema who suffer recurrent cutaneous staphylococcal infections may have defective neutrophil chemotaxis in association with increased IgE and have demonstrated that defective neutrophil function may result from chemical mediators such as histamine. The present patients with clinical evidence of systemic histamine release, abnormal chemotaxis and severe staphylococcal infections suggest an important relationship between allergic phenomena and the host defense mechanism.

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