IgA-related defective neutrophil chemotaxis in ulcerative colitis.

A case of ulcerative colitis with defective neutrophil chemotaxis, improved after short sulfasalazine therapy, is reported. This is the first case of this disease in which the chemotactic defect was characterized as a serum inhibitor, directed toward autologous and homologous neutrophils and associated with circulating IgA. Preincubation of normal neutrophils with increasing concentrations of patient's serum resulted in a dose-related inhibition, suggesting a stoichiometric relationship between humoral inhibitory power and neutrophils.