van Putten J P
Max-Planck-Institut für Biologie, Abt. Infektionsbiologie, Tübingen, Germany.
EMBO J. 1993 Nov;12(11):4043-51. doi: 10.1002/j.1460-2075.1993.tb06088.x.
Phase variation of Neisseria gonorrhoeae lipopolysaccharide (LPS) controls both bacterial entry into human mucosal cells, and bacterial susceptibility to killing by antibodies and complement. The basis for this function is a differential sialylation of the variable oligosaccharide moiety of the LPS. LPS variants that incorporate low amounts of sialic acid enter human mucosal epithelial cells very efficiently, but are susceptible to complement-mediated killing. Phase transition to a highly sialylated LPS phenotype results in equally adhesive but entry deficient bacteria which, however, resist killing by antibodies and complement because of dysfunctional complement activation. Phase variation of N. gonorrhoeae LPS thus functions as an adaptive mechanism enabling bacterial translocation across the mucosal barrier, and, at a later stage of infection, escape from the host immune defence.
淋病奈瑟菌脂多糖（LPS）的相变既控制细菌进入人黏膜细胞，也控制细菌对抗体和补体杀伤作用的敏感性。这种功能的基础是LPS可变寡糖部分的唾液酸化差异。掺入少量唾液酸的LPS变体能够非常有效地进入人黏膜上皮细胞，但易受补体介导的杀伤作用。向高唾液酸化LPS表型的相变导致细菌具有同等的黏附性但进入细胞的能力缺陷，然而，由于补体激活功能失调，这些细菌能够抵抗抗体和补体的杀伤。因此，淋病奈瑟菌LPS的相变作为一种适应性机制，使细菌能够穿过黏膜屏障进行转移，并在感染后期逃避宿主的免疫防御。
