SURFACE-CONTACT INHIBITS NEUTROPHIL SUPEROXIDE GENERATION INDUCED BY SOLUBLE STIMULI

  • 1 January 1985
    • journal article
    • research article
    • Vol. 52  (5) , 515-522
Abstract
Human neutrophils in suspension undergo a metabolic burst and generate reactive O2- metabolites upon exposure to many soluble and particulate stimuli. They can also be stimulated to produce O2- when in contact with surfaces. When neutrophils were allowed to settle onto protein-coated surfaces the amount of O2- they generated varied with the nature of the protein: IgG > bovine serum albumin > plastic > gelatin > serum > collagen. However, when polymorphonuclear leukocytes were permitted to settle onto a surface and then were stimulated with either phorbol myristate acetate or N-formyl-methionyl-leucyl-phenylalanine the O2- response was greatly diminished compared to control cells that were exposed to the stimulus in suspension. In contrast, superoxide production in response to the particulate stimulus opsonized zymosan was similar in both suspended and settled neutrophils. The degree of inhibition was not related to the degree of adherence since the diminished response occurred with all of the surfaces tested and in the presence of cytochalasin B. Onset of inhibition was very rapid as was recovery when cells were resuspended. Whereas production of O2- was greatly inhibited by surface contact, release of lysosomal enzymes were only slightly affected. The effect of surface contact did not appear to be mediated via activation of adenylate cyclase since the combination of a phosphodiesterase inhibitor and exogenous dibuteryl cyclic adenosine monophosphate did not inhibit phorbol myristate acetate O2- production, but surface contact did. Surface contact such as would occur during diapedesis and chemotaxis profoundly alters neutrophils behavior by an unknown mechanism and observations made on polymorphonuclear leukocytes in suspension cannot be generalized to polymorphonuclear leukocytes in tissue.