近日,，國(guó)際著名雜志PLoS Pathogens在線刊登了瑞士蘇黎世聯(lián)邦理工學(xué)院研究者的最新研究成果“Near Surface Swimming of Salmonella Typhimurium Explains Target-Site Selection and Cooperative Invasion”，文章中,，研究者揭示了泳動(dòng)現(xiàn)象或更易于鼠傷寒沙門菌進(jìn)行感染靶點(diǎn)的選擇,。
鼠傷寒沙門菌（S. Typhimurium）是一種重要的人畜共患病原菌，其感染發(fā)病率居沙門菌感染的首位,，常見于嬰幼兒發(fā)病,，而且可引發(fā)醫(yī)院感染和暴發(fā)性食物中毒，病死率非常之高,。以特許進(jìn)入位點(diǎn)為靶點(diǎn)是細(xì)菌感染的重要一步,，目前這種目標(biāo)機(jī)制并不清楚。
因此,，文章中,，研究者分析了S. Typhimurium的靶位選擇性，這種腸病源細(xì)菌擁有細(xì)菌細(xì)胞表面配基和三型分泌系統(tǒng),，對(duì)于結(jié)合宿主非常重要,，往往可以引發(fā)疾病。
使用建立好的組織模型培養(yǎng)系統(tǒng),，研究者發(fā)現(xiàn)了鞭毛驅(qū)使的運(yùn)動(dòng)可以促使細(xì)菌發(fā)生泳動(dòng)（swimming motility）,，這就使得細(xì)菌更加容易掃描到宿主表面，從而進(jìn)行吸附,，進(jìn)一步感染,。這種表面泳動(dòng)現(xiàn)象是細(xì)菌獨(dú)特的拓?fù)鋵W(xué)特性，如圓細(xì)胞和細(xì)胞褶皺,。這也就解釋了S. Typhimurium如何識(shí)別特殊的把微點(diǎn)來吸附至宿主細(xì)胞膜從而引發(fā)感染,。
更有意思的是，細(xì)菌這種泳動(dòng)是通過特殊的物理原理來引發(fā)的運(yùn)動(dòng),，因此,，研究者的研究發(fā)現(xiàn)為能動(dòng)致病菌的感染以及其治療提供了一定的思路,。（生物谷Bioon.com）
doi:10.1371/journal.ppat.1002810
PMC:
PMID:
Near Surface Swimming of Salmonella Typhimurium Explains Target-Site Selection and Cooperative Invasion
Benjamin Misselwitz1#, Naomi Barrett1#, Saskia Kreibich1, Pascale Vonaesch1, Daniel Andritschke1, Samuel Rout1, Kerstin Weidner1, Milos Sormaz2, Pascal Songhet1, Peter Horvath3, Mamta Chabria4, Viola Vogel4, Doris M. Spori2, Patrick Jenny5, Wolf-Dietrich Hardt1*
Targeting of permissive entry sites is crucial for bacterial infection. The targeting mechanisms are incompletely understood. We have analyzed target-site selection by S. Typhimurium. This enteropathogenic bacterium employs adhesins (e.g. fim) and the type III secretion system 1 (TTSS-1) for host cell binding, the triggering of ruffles and invasion. Typically, S. Typhimurium invasion is focused on a subset of cells and multiple bacteria invade via the same ruffle. It has remained unclear how this is achieved. We have studied target-site selection in tissue culture by time lapse microscopy, movement pattern analysis and modeling. Flagellar motility (but not chemotaxis) was required for reaching the host cell surface in vitro. Subsequently, physical forces trapped the pathogen for ~1.5–3 s in “near surface swimming”. This increased the local pathogen density and facilitated “scanning” of the host surface topology. We observed transient TTSS-1 and fim-independent “stopping” and irreversible TTSS-1-mediated docking, in particular at sites of prominent topology, i.e. the base of rounded-up cells and membrane ruffles. Our data indicate that target site selection and the cooperative infection of membrane ruffles are attributable to near surface swimming. This mechanism might be of general importance for understanding infection by flagellated bacteria.
