Linear gramicidin activates neutrophil functions and the activation is blocked by chemotactic peptide receptor antagonist.
The activation of functional responses in rabbit peritoneal neutrophils by gramicidin and the chemotactic peptide, N-formyl-methionyl-leucyl-phenylalanine methyl ester, was studied. Gramicidin activated superoxide generation, lysosomal enzyme release and a decrease in fluorescence of chlortetracycline-loaded cells, as for the chemotactic peptide. The maximum intensities of the responses by gramicidin were lower than that by chemotactic peptide. Responses by both these peptides could be inhibited by t-butyloxycarbonyl-methionyl-leucyl-phenylalanine, a chemotactic peptide receptor antagonist. Gramicidin gave responses at low doses comparable to that of the chemotactic peptide.
D000818:Animals; D002751:Chlortetracycline; D006096:Gramicidin / Q000494:pharmacology*; D007700:Kinetics; D008247:Lysosomes / Q000201:enzymology; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000378:metabolism / Q000494:pharmacology; D009504:Neutrophils / Q000187:drug effects / Q000502:physiology*; D009842:Oligopeptides / Q000494:pharmacology*; D011817:Rabbits; D044042:Receptors, Formyl Peptide; D011971:Receptors, Immunologic / Q000187:drug effects / Q000502:physiology*; D013050:Spectrometry, Fluorescence; D013481:Superoxides / Q000378:metabolism
D009842:Oligopeptides; D044042:Receptors, Formyl Peptide; D011971:Receptors, Immunologic; D013481:Superoxides; D006096:Gramicidin; D009240:N-Formylmethionine Leucyl-Phenylalanine; C046832:t-butyloxycarbonyl-methionyl-leucyl-phenylalanine; D002751:Chlortetracycline