在2007年12月13日的《細(xì)胞—宿主與微生物》（Cell Host & Microbe）的封面文章中，德國馬普傳染生物學(xué)研究所的Cindy Rechner等人發(fā)現(xiàn),，宿主糖蛋白Gp96和清道夫受體SREC在奈瑟氏淋球菌入侵時(shí)會(huì)特異性地與淋球菌的一些蛋白發(fā)生作用,。
奈瑟氏淋球菌感染宿主時(shí)會(huì)表達(dá)出許多蛋白質(zhì)來調(diào)節(jié)細(xì)菌的粘附和入侵。Rechner研究的奈瑟氏淋球菌表達(dá)的血清A型主要外膜蛋白PorBIA取自于患有重癥感染疾病的患者,。在類似全身血液感染的低濃度磷酸鹽條件下,，PorBIA能夠有效啟動(dòng)侵襲細(xì)菌的粘附和侵襲作用。
同時(shí),，Rechner等研究發(fā)現(xiàn)人熱休克糖蛋白Gp96和清道夫受體SREC是PorBIA的特異性受體,。奈瑟氏淋球菌表達(dá)的血清A型蛋白PorBIA（注意不是血清B型蛋白PorB）特異性地結(jié)合在宿主或重組的人熱休克糖蛋白Gp96上。宿主細(xì)胞Gp96的枯竭會(huì)阻止粘附,，卻會(huì)有效引發(fā)奈瑟氏淋球菌的侵入,。這種入侵會(huì)被化學(xué)抑制劑清道夫受體阻斷，清道夫受體SREC能夠特異性地阻斷PorBIA的侵入,。
因此,，Rechner等人認(rèn)為，宿主細(xì)胞中的熱休克糖蛋白Gp96可以抵抗奈瑟氏球菌的入侵,，而清道夫受體SREC能夠介導(dǎo)宿主細(xì)胞的進(jìn)入,，從而阻斷細(xì)菌粘附和侵襲。（科學(xué)網(wǎng) 武彥文/編譯）
原始出處:
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
[email protected]
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.
