Isoproterenol inhibition of isolated human neutrophil function.
The human PMN can contribute to the inflammatory response. Several neutrophil responses can be inhibited by agonists that increase the cellular levels of cyclic AMP. In the following article, we compared the effects of ISO on lysosomal beta-glucuronidase release, superoxide generation, and CL in isolated human PMNs. ISO inhibited the neutrophil CL response to opsonized zymosan in a dose-dependent fashion with maximal effects at 10(-4)M. ISO inhibition of CL was not enhanced by the addition of theophylline, nor was CL inhibited by the exogenous addition cyclic AMP except at a very high concentration of 10(-3)M. ISO also suppressed beta-glucuronidase release and superoxide generation in neutrophils during an incubation with opsonized zymosan particles. For ISO to inhibit beta-glucuronidase release and superoxide generation, theophylline (5 X 10(-4)M) was necessary. ISO effectively inhibits three neutrophil functions that are capable of causing tissue inflammation. Although ISO suppressed all three neutrophil responses, the inhibitory mechanisms appear to be variable.
D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002469:Cell Separation; D000242:Cyclic AMP / Q000494:pharmacology; D004837:Epinephrine / Q000494:pharmacology; D005966:Glucuronidase / Q000037:antagonists & inhibitors; D006801:Humans; D007545:Isoproterenol / Q000494:pharmacology*; D008163:Luminescent Measurements; D009504:Neutrophils / Q000201:enzymology / Q000276:immunology* / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism; D015054:Zymosan / Q000494:pharmacology
D000893:Anti-Inflammatory Agents; D013481:Superoxides; D015054:Zymosan; D000242:Cyclic AMP; D005966:Glucuronidase; D007545:Isoproterenol; D004837:Epinephrine