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Department of Physiology and Cellular Biophysics, Columbia University College of Physicians and Surgeons, New York, New York
Correspondence: John D. Loike, Department of Physiology and Cellular Biophysics, Columbia University College of Physicians and Surgeons, 650 W. 168th St., New York, NY 10027. E-mail: jdl5{at}columbia.edu
fMLP- or TNF-
-stimulated neutrophils produced H2O2 when they adhered to fibrinogen-coated surfaces but not when they adhered to collagen I-, collagen IV-, or Matrigel-coated surfaces. In contrast, LTB4- or IL-8-stimulated neutrophils did not produce H2O2 when they adhered to any of these surfaces. fMLP and TNF- were much more potent than LTB4 and IL-8 in stimulating neutrophils to up-regulate and to activate their Mß2 integrins, as measured by the binding of specific monoclonal antibodies. Pretreatment of neutrophils with pertussis toxin completely blocked their production of H2O2 on fibrinogen-coated surfaces in response to fMLP and their migration through Matrigel in response to fMLP, LTB4, and IL-8. These data show that although the fMLP, LTB4, and IL-8 receptors are coupled to pertussis toxin-sensitive G proteins, they signal neutrophils to initiate qualitatively different effector functions. We propose that the qualitative differences in effector functions signaled by different chemoattractants reflect qualitative differences in using G-protein ß and/or 
subunits or other factors by their cognate receptors.
Key Words: H2O2 • fMLP • LTB4 • integrins • fibrin
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