Lack of a central role for calcium in the induction and release of human interleukin-1.
This study examines the potential role of calcium in the activation of human monocytes by bacterial lipopolysaccharide (LPS) to produce interleukin-1 (IL-1). Monocytes cannot be triggered to produce IL-1 through addition of calcium ionophores. Triggering of IL-1 production by LPS cannot be blocked by depletion of extracellular calcium, blockade of calcium channels, or addition of agents which antagonize the effects of intracellular calcium. Finally, the addition of LPS does not induce the mobilization of intracellular free calcium as measured by quin-2 fluorescence.
D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000502:physiology*; D002451:Cell Compartmentation; D002746:Chlorpromazine / Q000494:pharmacology; D004987:Ethers / Q000494:pharmacology; D005110:Extracellular Space / Q000502:physiology; D005707:Gallic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D006801:Humans; D007375:Interleukin-1 / Q000378:metabolism*; D007473:Ion Channels / Q000502:physiology; D015759:Ionomycin; D008070:Lipopolysaccharides / Q000494:pharmacology; D008262:Macrophage Activation; D009000:Monocytes / Q000502:physiology*; D014268:Trifluoperazine / Q000494:pharmacology
D004987:Ethers; D007375:Interleukin-1; D007473:Ion Channels; D008070:Lipopolysaccharides; D014268:Trifluoperazine; D000001:Calcimycin; D015759:Ionomycin; C006014:8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate; D005707:Gallic Acid; D002118:Calcium; D002746:Chlorpromazine