| First Author | Richardson SH | Year | 1993 |
| Journal | Clin Infect Dis | Volume | 16 Suppl 2 |
| Pages | S83-91 | PubMed ID | 8452965 |
| Mgi Jnum | J:12238 | Mgi Id | MGI:60488 |
| Doi | 10.1093/clinids/16.supplement_2.s83 | Citation | Richardson SH, et al. (1993) Biochemical and genetic basis for the ETS (enterotoxin sensitivity) phenotype in mice. Clin Infect Dis 16 Suppl 2:S83-91 |
| abstractText | Evidence has been accumulating that humans are genetically predisposed to cholera gravis. Using the sealed adult mouse model, we found that certain inbred mice were also hypersensitive to cholera toxin (CT). Such mice were designated ETS+ (enterotoxin sensitive), and the trait was linked to the K end of the mouse H-2 histocompatibility complex. Cells isolated from ETS+ mice bound more CT and accumulated more cyclic adenosine monophosphate (cAMP) after intoxication. Analysis of ETS+ cells showed that they express lesser amounts of the non-GM1 gangliosides that block or compete for relevant CT binding sites in ETS- cells. Conversion of ETS- non-GM1 gangliosides to GM1 with neuraminidase increased CT binding and cAMP responses. Reconstitution of nonreactive ganglioside-deficient cells with ETS+ or ETS- gangliosides caused them to bind CT like the original ETS+ or ETS- cells. Ganglioside expression genes known to map to the same H-2-linked region as the ETS phenotype seem to be involved in controlling murine susceptibility to CT. |
