Defective monocyte and polymorphonuclear leukocyte chemotaxis in atopic disease.

Monocyte (MN) and polymorphonuclear (PMN) leukocyte chemotaxis was studied in 17 atopic children with hyperimmunoglobulinemia E (IgE), 9 age- and diagnosis-matched children with normal IgE levels, 10 pediatric controls, and 45 adult controls. Twenty-one of the 26 atopic patients had eczema, while 5 had only respiratory allergies. All patients were free of infection and receiving no systemic corticosteroids. Depressed PMN chemotaxis was found in only one patient. Defects of MN chemotaxis were detected in 8 of 17 atopic children with IgE and 2 of 9 with normal IgE values. Seven of 21 patients with atopic eczema and 3 of 5 with respiratory allergies had depressed MN chemoatxis. No evidence was found for a cell-directed chemotactic inhibitor in the plasma of patients with abnormal MN chemotaxis. These data demonstrate that: (1) MN chemotaxis is frequently depressed in uninfected atopic patients; (2) this abnormality occurs in patients with respiratory allergies as well as in those with eczema and is more prevalent in atopics with IgE; and (3) PMN chemotactic defects are uncommon in allergic patients. Whether abnormal MN chemotaxis is a primary or a secondary event in atopy requires further investigation.