Bradykinin stimulates tumor necrosis factor and interleukin-1 release from macrophages.
Bradykinin and related kinins have been implicated in the initiation and maintenance of inflammation. Cytokines appear to be the primary mediators of many inflammatory diseases. The potential ability of bradykinin to stimulate release of tumor necrosis factor and interleukin-1 from macrophages was examined. Bradykinin stimulated release of both cytokines from P388-D1 and RAW264.7 murine macrophages. Studies with selective agonists and antagonists suggest that cytokine release is mediated by a B1 kinin receptor.
Tiffany
C W
CW
Nova Pharmaceutical Corporation, Baltimore, MD 21224.
Burch
R M
RM
D000818:Animals; D001920:Bradykinin / Q000031:analogs & derivatives / Q000494:pharmacology*; D002460:Cell Line; D007375:Interleukin-1 / Q000378:metabolism*; D008071:Lipoprotein Lipase / Q000037:antagonists & inhibitors; D008264:Macrophages / Q000378:metabolism*; D051379:Mice; D011458:Prostaglandins E / Q000096:biosynthesis; D018002:Receptors, Bradykinin; D017981:Receptors, Neurotransmitter / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D007375:Interleukin-1; D011458:Prostaglandins E; D018002:Receptors, Bradykinin; D017981:Receptors, Neurotransmitter; D014409:Tumor Necrosis Factor-alpha; C024626:bradykinin, des-Arg(9)-; D008071:Lipoprotein Lipase; D001920:Bradykinin