[Effects of pepstatin A on neutrophils; cross-deactivation with FMLP].
The ability of pepstatin A, a protease inhibitor produced by Streptomyces testaceus, to elicit a number of responses by the human PMN has been studied. In lysozyme and beta-glucuronidase release, pepstatin A 10(-5)M is equivalent to the synthetic oligopeptide N-formyl-methionyl-leucyl-phenylalanine (FMLP) 10(-7)M. In superoxide release, pepstatin A 10(-5)M produces 80% of that originated by FMLP 10(-7). After two minutes of incubation the superoxide release is important, there being no further increase after 10 minutes. Preincubation of the cells with cytochalasin B before stimulation with pepstatin A elicits a noticeable increase in O2- release. In chemotaxis, pepstatin A 10(-6) originates the same cell motility as FMLP 10(-9). Pepstatin A produces a cross deactivation with FMLP which adds further evidence to the hypothesis that both stimuli compete for the same receptor in the PMN.
Muniain
M A
MA
Pozuelo
F
F
Pérez-Venegas
J J
JJ
Romero-Tabares
A
A
Rodríguez-Hornillo
M C
MC
Garrido
M
M
D001667:Binding, Competitive; D002634:Chemotaxis, Leukocyte / Q000187:drug effects; D003571:Cytochalasin B / Q000494:pharmacology; D003574:Cytochrome c Group / Q000378:metabolism; D005966:Glucuronidase / Q000378:metabolism; D006801:Humans; D009113:Muramidase / Q000378:metabolism; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology; D009504:Neutrophils / Q000187:drug effects* / Q000502:physiology; D009842:Oligopeptides / Q000494:pharmacology*; D010436:Pepstatins / Q000494:pharmacology*; D044042:Receptors, Formyl Peptide; D011971:Receptors, Immunologic / Q000187:drug effects; D013481:Superoxides / Q000378:metabolism
D003574:Cytochrome c Group; D009842:Oligopeptides; D010436:Pepstatins; D044042:Receptors, Formyl Peptide; D011971:Receptors, Immunologic; D013481:Superoxides; C014195:Streptomyces pepsin inhibitor; D003571:Cytochalasin B; D009240:N-Formylmethionine Leucyl-Phenylalanine; D009113:Muramidase; D005966:Glucuronidase; C031375:pepstatin
Efectos de la pepstatina A sobre los neutrófilos; desactivación cruzada con el FMLP.