美國佛羅里達(dá)中央大學(xué)的微生物學(xué)教授Keith Ireton的科研小組發(fā)現(xiàn)了致死性食源性細(xì)菌一個(gè)先前未被了解的的傳播機(jī)制,。
李斯特氏菌（Listeria monocytogenes）是一種細(xì)菌,。它會導(dǎo)致懷孕婦女流產(chǎn)，在老年人和免疫系統(tǒng)損傷人群中引起腦膜炎,。2002年在美國多個(gè)州就爆發(fā)了利斯特氏菌病。
研究至今,，科學(xué)家已經(jīng)知道利斯特菌會從人類的一個(gè)細(xì)胞傳遞到另一個(gè)細(xì)胞,，即它能夠快速地感染其相鄰細(xì)胞。
在這項(xiàng)研究中,，Ireton的研究小組發(fā)現(xiàn)了一個(gè)之前未知的過程,，該過程能夠幫助細(xì)菌感染健康細(xì)胞。這項(xiàng)研究結(jié)果發(fā)表在本周的Nature Cell Biology上,。
健康人類細(xì)胞的脂膜通常處于緊張的狀態(tài),，這種狀態(tài)可以阻止利斯特菌到相鄰未被感染細(xì)胞的傳播。然而,，在實(shí)驗(yàn)室中,，研究人員發(fā)現(xiàn)，利斯特菌的一種叫InIC的蛋白，似乎緩解了感染細(xì)胞脂膜的張力,，使脂膜更易變形而有利于細(xì)菌的轉(zhuǎn)移,，隨后進(jìn)入相鄰的健康細(xì)胞。
Ireton的實(shí)驗(yàn)室還發(fā)現(xiàn),，InIC緩解張力的方式是通過阻礙人類細(xì)胞中一種叫Tuba的蛋白的活性,。Tuba正常的作用是幫助脂膜產(chǎn)生張力，而利斯特菌蛋白InIC阻礙了Tuba蛋白的活性,，減緩了張力使細(xì)菌能夠傳播到附近的健康細(xì)胞,。
這項(xiàng)關(guān)于病原菌通過控人類細(xì)胞脂膜張力進(jìn)行傳播的研究還沒有科學(xué)文獻(xiàn)描述，所以該發(fā)現(xiàn)可能有助于其他的細(xì)菌性病原菌的研究,，如志賀氏菌等,，同時(shí)也為未來相關(guān)疾病的治療以及細(xì)菌性病原菌導(dǎo)致疾病的機(jī)制的理解開辟了道路。
研究人員指出,，接下來他們還需要進(jìn)行更多深入的研究,。（生物谷bioon.com）
生物谷推薦原始出處：
Nature Cell Biology 20 September 2009 | doi:10.1038/ncb1964
The bacterial virulence factor InlC perturbs apical cell junctions and promotes cell-to-cell spread of Listeria
Tina Rajabian1, Balramakrishna Gavicherla2, Martin Heisig3, Stefanie Müller-Altrock4, Werner Goebel4, Scott D. Gray-Owen1 & Keith Ireton2
Several pathogenic bacteria, including Listeria monocytogenes, use an F-actin motility process to spread between mammalian cells1. Actin 'comet tails' propel Listeria through the cytoplasm, resulting in bacteria-containing membrane protrusions that are internalized by neighbouring cells. The mechanism by which Listeria overcomes cortical tension to generate protrusions is unknown. Here, we identify bacterial and host proteins that directly regulate protrusions. We show that efficient spreading between polarized epithelial cells requires the secreted Listeria virulence protein InlC (internalin C). We next identify the mammalian adaptor protein Tuba as a ligand of InlC. InlC binds to a carboxy-terminal SH3 domain in Tuba, which normally engages the human actin regulatory protein N-WASP2. InlC promotes protrusion formation by inhibiting Tuba and N-WASP activity, probably by impairing binding of N-WASP to the Tuba SH3 domain. Tuba and N-WASP are known to control the structure of apical junctions in epithelial cells3. We demonstrate that, by inhibiting Tuba and N-WASP, InlC makes taut apical junctions become slack. Experiments with myosin II inhibitors indicate that InlC-mediated perturbation of apical junctions accounts for the role of this bacterial protein in protrusion formation. Collectively, our results suggest that InlC promotes bacterial dissemination by relieving cortical tension, thereby enhancing the ability of motile bacteria to deform the plasma membrane into protrusions.
1 Department of Molecular Genetics, University of Toronto. Toronto, Ontario, M5S 1A8, Canada.
2 Department of Molecular Biology and Microbiology, College of Medicine, Burnett School of Biomedical Sciences, University of Central Florida, Orlando, FL 32826-3227, USA.
3 Institute for Medical Radiation and Cell Research (MSZ), University of Würzburg, 97078, Würzburg, Germany.
4 Biocenter (Microbiology), University of Würzburg, 97074 Würzburg, Germany.
