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Infect Immun. 1990 September; 58(9): 2888-2894

Altered B-lymphocyte membrane architecture indicated by ganglioside accessibility in C3H/HeJ mice.

Department of Internal Medicine, Yale University School of Medicine, West Haven, Connecticut.

ABSTRACT

We have analyzed both the total ganglioside composition and the surface accessibility of C3H/HeN B lymphocytes and C3H/HeJ B lymphocytes. Seventeen individual resorcinol-positive moieties were visualized by two-dimensional thin-layer chromatography of the purified gangliosides from both strains. Complete homology between strains was seen in the patterns of total gangliosides purified from the endotoxin-responsive and -hyporesponsive strains, with only minor differences in the relative concentrations of four gangliosides. In comparison, only 12 individual gangliosides were accessible to surface labeling following galactose oxidase treatment in these same strains, suggesting that some gangliosides are masked at the cell surface in both strains. However, labeling of the more polar components was greatly reduced in the endotoxin-hyporesponsive (C3H/HeJ) strain, suggesting that these gangliosides have decreased accessibility to galactose oxidase at the cell surface. Therefore, while the total ganglioside compositions of the two strains were nearly equivalent, there were dramatic differences in ganglioside surface accessibility. These findings indicate that an alteration in membrane structure that is associated with the endotoxin hyporesponsiveness observed in C3H/HeJ B lymphocytes exists.

This article has been cited by other articles:

• Berenson, C. S., Rasp, R. H., Gau, J.-T., Ryan, J. L., Yohe, H. C. (2001). Differences in splenic B-lymphocyte ganglioside expression and accessibility in normal and endotoxin-hyporesponsive mice. J. Leukoc. Biol. 69: 969-976 [Abstract] [Full Text]  
• Yohe, H. C., Griffin, M. E. (1997). Reduction of asialo pathway gangliosides in Escherichia coli-activated peritoneal macrophages from endotoxin hyporesponsive mice. Innate Immunity 4: 401-408 [Abstract]