Abstract

Cellular and/or serum components of polymorphonuclear leucocyte chemotaxis were assessed in 21 patients with rheumatoid arthritis. No difference in the chemotactic migration of control and patient cells in response to a number of chemotactic solutions could be detected (P = 0.38). Deficient generation of chemotactic activity in patient sera (P = 0.58) as compared to control sera (P = 0.014) after incubation of the sera with Escherichia coli lipopolysaccharide, resulted in a significant difference in the chemotactic activity of the control and rheumatoid serum preparations for polymorphonuclear leucocytes (P = 0.0012). This defect was associated with the presence of a serum inhibitor of chemotaxis, the potency of which was inversely correlated with the level of chemotactic activity generated in the rheumatoid sera (r = -0.941, P less than 0.001).