Met-enkephalin induced alterations of macrophage functions.
Met-enkephalin /Met-enk/ was found to stimulate IgG2a-mediated antibody dependent cytotoxicity /ADCC/ of thioglycollate elicited rat peritoneal macrophages /PM/ through naloxone-sensitive opiate receptors in concentrations ranging from 10(-9) - 14(-7) M. Phagocytosis of IgG2a coated 51Cr-sheep red blood cell /SRBC/ was suppressed by M-enk in the same concentration range. In the same range of concentrations, M-enk was observed to induce a significant increase in the generation of luminol dependent chemiluminescence /LDCL/. The observed stimulation of ADCC was abolished by calmodulin inhibitor triflouroperazine /TFP/ in 10(-6) M concentration. The involvement of cyclic nucleotides in the M-enk induced functional alterations is indicated by finding cGMP accumulation to be augmented in M-enk treated PMs.
D000818:Animals; D000920:Antibody-Dependent Cell Cytotoxicity / Q000187:drug effects; D002147:Calmodulin / Q000037:antagonists & inhibitors; D006152:Cyclic GMP / Q000032:analysis; D004744:Enkephalin, Methionine / Q000494:pharmacology*; D008163:Luminescent Measurements; D008165:Luminol / Q000378:metabolism; D008264:Macrophages / Q000187:drug effects* / Q000201:enzymology / Q000276:immunology; D008297:Male; D010587:Phagocytosis / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains; D014268:Trifluoperazine / Q000494:pharmacology
D002147:Calmodulin; D014268:Trifluoperazine; D004744:Enkephalin, Methionine; D008165:Luminol; D006152:Cyclic GMP