[转移贴]宿主细胞如何应对奈瑟氏球菌入侵

ms003

原贴由zhangning发表于 2008-1-5 17:50
http://biosky.haotui.com/thread-3007-1-5.html

在2007年12月13日的《细胞—宿主与微生物》（Cell  Host  &  Microbe）的封面文章中，德国马普传染生物学研究所的Cindy  Rechner等人发现，宿主糖蛋白Gp96和清道夫受体SREC在奈瑟氏淋球菌入侵时会特异性地与淋球菌的一些蛋白发生作用。   

奈瑟氏淋球菌感染宿主时会表达出许多蛋白质来调节细菌的粘附和入侵。Rechner研究的奈瑟氏淋球菌表达的血清A型主要外膜蛋白PorBIA取自于患有重症感染疾病的患者。在类似全身血液感染的低浓度磷酸盐条件下，PorBIA能够有效启动侵袭细菌的粘附和侵袭作用。   

同时，Rechner等研究发现人热休克糖蛋白Gp96和清道夫受体SREC是PorBIA的特异性受体。奈瑟氏淋球菌表达的血清A型蛋白PorBIA（注意不是血清B型蛋白PorB）特异性地结合在宿主或重组的人热休克糖蛋白Gp96上。宿主细胞Gp96的枯竭会阻止粘附，却会有效引发奈瑟氏淋球菌的侵入。这种入侵会被化学抑制剂清道夫受体阻断，清道夫受体SREC能够特异性地阻断PorBIA的侵入。   

因此，Rechner等人认为，宿主细胞中的热休克糖蛋白Gp96可以抵抗奈瑟氏球菌的入侵，而清道夫受体SREC能够介导宿主细胞的进入，从而阻断细菌粘附和侵袭。（科学网 武彦文/编译）

原始出处:



Cell Host and Microbe, Vol 2, 393-403, 13 December 2007

Host Glycoprotein Gp96 and Scavenger Receptor SREC Interact with PorB of Disseminating Neisseria gonorrhoeae in an Epithelial Invasion Pathway

Cindy Rechner,1 Christiane Kühlewein,1 Anne Müller,3 Hansjörg Schild,2 and Thomas Rudel1,

1 Max Planck Institute for Infection Biology, Department of Molecular Biology, Research Group for Molecular Infection and Cancer Biology, Charitéplatz 1, Berlin D-10117, Germany
2 Institute for Immunology, Johannes Gutenberg University Mainz, Mainz 55131, Germany


Corresponding author
Thomas Rudel
rudel@mpiib-berlin.mpg.de

Summary

Neisseria gonorrhoeae expresses numerous surface proteins that mediate bacterial adherence and invasion during infection. Gonococci expressing serotype A of the major outer membrane porin PorB (PorBIA) are frequently isolated from patients with severe disseminating infections. PorBIA triggers efficient adherence and invasion under low phosphate conditions mimicking systemic bloodstream infections. Here, we identify the human heat shock glycoprotein Gp96 and the scavenger receptor SREC as PorBIA-specific receptors. Gonococci expressing PorBIA, but not those expressing PorB serotype B instead, bind to purified native or recombinant Gp96. Depletion of Gp96 from host cells prevented adherence but significantly triggered gonococcal invasion. Furthermore, such invasion was blocked by chemical inhibitors of scavenger receptors, and we identified SREC as the scavenger receptor involved in PorBIA-dependant invasion. Thus, we establish Gp96 as an anti-invasion factor and SRECs as receptors mediating host cell entry of highly invasive disseminating gonococci.