Human neutrophils adherent to proteins derived from serum or plasma, or to the basement membrane protein laminin, underwent a delayed but massive respiratory burst in response to recombinant human CSF-GM or CSF-G. No such response was elicited from neutrophils in suspension. On a molar basis, CSF-GM (EC50 approximately 126 pmol/L) and CSF-G (EC50 approximately 585 pmol/L) were about as potent as TNF alpha and TNF beta in their elicitation of H2O2 release and orders of magnitude more potent than previously studied formylated peptides or C5a. CSF-GM and CSF-G prime suspended neutrophils for a respiratory burst in response to soluble agonists, such as formylated peptides. Compared to the CSF- primed respiratory burst of nonadherent neutrophils, the CSF-triggered response of adherent neutrophils is markedly more delayed in onset (73 to 95 minutes), prolonged in duration (150 to 180 minutes), and greater in extent (approximately 60 to 100 nmol H2O2 released/10(6) neutrophils). Neither CSF-M, interleukin-3 (IL-3), nor bacterial lipopolysaccharide triggered the respiratory burst in adherent neutrophils, nor did CSF-GM or CSF-G trigger a respiratory burst in adherent monocytes. Release of CSF-GM and CSF-G in response to antigens, bacterial products, or cytokines may give mononuclear cells control over the respiratory burst of noncirculating neutrophils during inflammatory and immune responses.

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