Priming of oxidative response in human neutrophils by anti-CD18 monoclonal antibodies.

Abstract

Type I collagen, the most abundant protein in the body, after acid extraction adheres to and can induce a respiratory burst from neutrophils. It has been proposed that the effects of collagen are mediated via the CD18 subfamily of integrins. In the present study, adhesion was measured by affinity chromatography in a column containing collagen-coated microcarriers, while oxygen metabolite production was measured with luminol-dependent chemiluminescence. Neutrophil adherence to collagen was attenuated by anti-CD18 monoclonal antibodies. The respiratory burst in response to collagen was not affected by the antibodies. Incubation of neutrophils with anti-CD18 antibodies prior to stimulation with FMLP increased both the extra- and intracellular respiratory burst. Treatment with antibodies prior to PMA stimulation increased only the extracellular respiratory burst. In conclusion, the respiratory burst from neutrophils is primed by pretreatment with anti-CD18 monoclonal antibodies. The collagen-stimulated respiratory burst is probably also primed, but the effect is hidden by the simultaneous attenuation of adhesion.