Gascoyne N, van Heyningen W E
J Infect Dis. 1979 Feb;139(2):235-6. doi: 10.1093/infdis/139.2.235.
Endongenous and exogenous sialidases appear to unmask sialidase-stable and sialidase-labile gangliosides in intestinal mucosal homogenates by attacking glycoproteins. Exogenous (but not endogenous) sialidase then converts sialidase-labile gangliosides into the cholera toxin-binding, sialidase-stable ganglioside GM1 (galactosyl-N-acetylgalactosaminyl [sialosyl] lactosyl ceramide). Since Vibrio cholerae produces sialidase, these observations may be relevant to the course of cholera.
内源性和外源性唾液酸酶似乎通过攻击糖蛋白来暴露肠黏膜匀浆中对唾液酸酶稳定和不稳定的神经节苷脂。然后外源性(而非内源性)唾液酸酶将对唾液酸酶不稳定的神经节苷脂转化为与霍乱毒素结合的、对唾液酸酶稳定的神经节苷脂GM1(半乳糖基-N-乙酰半乳糖胺基[唾液酸基]乳糖基神经酰胺)。由于霍乱弧菌产生唾液酸酶,这些观察结果可能与霍乱病程相关。