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PMID: 222809 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

Gangliosides sensitize unresponsive fibroblasts to Escherichia coli heat-labile enterotoxin.

The Journal of clinical investigation ·Vol. 64 ·No. 2 ·1979-08-00 ·Pages 381-4

Moss J, Garrison S, Fishman PH, Richardson SH

Abstract

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.

MeSH Terms
Animals Cell Line Cholera Toxin/pharmacology Cyclic AMP/metabolism Enterotoxins/pharmacology Escherichia coli Fibroblasts/drug effects,metabolism Gangliosides/pharmacology Hot Temperature Mice
Chemicals
Enterotoxins Gangliosides Cholera Toxin Cyclic AMP
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Moss J
Garrison S
Fishman P H
Richardson S H
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28 references, click to expand
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Article Info
Journal
The Journal of clinical investigation
Abbr.
J Clin Invest
ISSN
0021-9738
DOI
10.1172/JCI109472
Published
1979-08-00
Pages
381-4
Language
English
Region
United States
NLM ID
7802877
PMCID
PMC372129
Subset
IM
External Links
PubMed source DOI: 10.1172/JCI109472 PMC Full Text View journal details
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