Cholera toxin synergizes LPS- and IL-1 beta-induced PGE2 release: potential amplification systems in cholera.
Incubation of LPS/IL-1 beta and cholera toxin combinations resulted in a synergistic rise of immunoreactive and [3H]PGE2 released from HGFs. This interaction was not dependent on the type of LPS utilized; however, the cholera toxin enzymatic subunit was essential to the synergism. Intracellular cAMP concentrations paralleled PGE2 synthesized in response to LPS and cholera toxin. dBcAMP and forskolin incubated with LPS failed to demonstrate the synergistic rise of PGE2, suggesting elevated cAMP levels alone are insufficient for increased PGE2 synthesis. These findings demonstrate interactions between LPS/IL-1 beta and cholera toxin and support the potential for an expanded role of LPS and IL-1 beta in the pathogenesis of cholera.
Hill
S J
SJ
Department of Periodontics, University of Texas Health Science Center, San Antonio 78284.
Ebersole
J L
JL
D016718:Arachidonic Acid / Q000378:metabolism; D002478:Cells, Cultured; D002771:Cholera / Q000378:metabolism*; D002772:Cholera Toxin / Q000494:pharmacology*; D002851:Chromatography, High Pressure Liquid; D000242:Cyclic AMP / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism*; D004357:Drug Synergism; D005347:Fibroblasts / Q000378:metabolism; D006801:Humans; D007375:Interleukin-1 / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000633:toxicity*; D008297:Male; D011863:Radioimmunoassay
D007375:Interleukin-1; D008070:Lipopolysaccharides; D016718:Arachidonic Acid; D002772:Cholera Toxin; D000242:Cyclic AMP; D015232:Dinoprostone