Gangliosides sensitize unresponsive fibroblasts to Escherichia coli heat-labile enterotoxin.
Chemically transformed mouse fibroblasts did not raise their cyclic AMP level in response to Escherichia coli heat-labile enterotoxin. These fibroblasts did, however, incorporate exogenous mono-, di-, and trisialogangliosides. After the uptake of monosialoganglioside galactosyl-N-acetylgalactosaminyl-[N-acetylneuraminyl]-galactosylglucosylceramide (GM1), the cells responded to E. coli heat-labile enterotoxin. The di- and trisialogangliosides were considerably less effective. GM1, the putative cholera toxin (choleragen) receptor, has been implicated previously as the receptor for E. coli heat-labile enterotoxin based on the ability of the free ganglioside to inhibit the effects of toxin. This investigation establishes that the ganglioside, when incorporated into fibroblasts, serves a functional role in mediating the responsiveness to the toxin.
D000818:Animals; D002460:Cell Line; D002772:Cholera Toxin / Q000494:pharmacology; D000242:Cyclic AMP / Q000378:metabolism*; D004768:Enterotoxins / Q000494:pharmacology*; D004926:Escherichia coli; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism*; D005732:Gangliosides / Q000494:pharmacology*; D006358:Hot Temperature; D051379:Mice
D004768:Enterotoxins; D005732:Gangliosides; D002772:Cholera Toxin; D000242:Cyclic AMP