Merz A J, So M
Department of Molecular Microbiology and Immunology, Oregon Health Sciences University, Portland 97201-3098, USA.
Infect Immun. 1997 Oct;65(10):4341-9. doi: 10.1128/iai.65.10.4341-4349.1997.
Attachment of piliated Neisseria gonorrhoeae or Neisseria meningitidis cells to A431, Chang, HEC-1-B, or polarized T(84) cells triggers rearrangements of cortical microfilaments and the accumulation of phosphotyrosine-containing proteins at sites of bacterial contact. Actin stress fibers and the microtubule network remain unaltered in infected cells. The rearrangements reported here are triggered by piliated, Opa- and Opc- strains and also by nonpiliated gonococci (GC) that produce the invasion-associated OpaA protein. Thus, neisserial adhesion via either of at least two different adhesins can trigger cortical rearrangements. In contrast, these rearrangements are not triggered by nonadherent GC or meningococcal strains, by heat-killed or chloramphenicol-treated GC strains, or by Escherichia coli recombinants that adhere to cells via GC OpaA or Opal fusion proteins, suggesting that additional neisserial components are involved. Immunoblotting experiments did not detect consistent increases in the phosphorylation of specific proteins. Possible biological implications of these Neisseria-induced cortical rearrangements are discussed.
具菌毛的淋病奈瑟菌或脑膜炎奈瑟菌细胞附着于A431、Chang、HEC - 1 - B或极化的T(84)细胞会引发皮质微丝的重排以及含磷酸酪氨酸蛋白在细菌接触位点的积累。在受感染的细胞中，肌动蛋白应激纤维和微管网络保持不变。此处报道的重排由具菌毛、Opa和Opc菌株引发，也由产生侵袭相关OpaA蛋白的非具菌毛淋病奈瑟菌（GC）引发。因此，通过至少两种不同黏附素中的任何一种进行的奈瑟菌黏附都可引发皮质重排。相比之下，这些重排不会由非黏附性GC或脑膜炎奈瑟菌菌株、热灭活或氯霉素处理的GC菌株，或通过GC OpaA或Opal融合蛋白黏附于细胞的大肠杆菌重组体引发，这表明还涉及其他奈瑟菌成分。免疫印迹实验未检测到特定蛋白磷酸化的一致增加。讨论了这些奈瑟菌诱导的皮质重排可能的生物学意义。
