This photo shoes bacterial colonies in a culture in the laboratory. Credit: João Gama & Francisco Dionísio, IGC & Univ. Lisbon
為什么結(jié)核分枝桿菌僅僅有為數(shù)不多的細(xì)菌便可以引起肺結(jié)核,，為什么霍亂弧菌必須在宿主內(nèi)注入數(shù)以百萬計(jì)的菌體才能夠引起霍亂呢,？近日，來自法國(guó)和葡萄牙的兩個(gè)研究小組共同在近日的一篇研究報(bào)告中回答了此問題,，研究人員表示,，可以侵入或者破壞人體免疫系統(tǒng)細(xì)胞的細(xì)菌具有很高的感染性,，因?yàn)檫@些細(xì)菌可以自由移動(dòng)、復(fù)制速度很快,，而且細(xì)菌之間可以進(jìn)行有效交流,，這樣就可以將很多細(xì)菌組織起來引起嚴(yán)重的感染，研究者的研究對(duì)于理解細(xì)菌感染的類別有著重要的作用,，而且可以精確的預(yù)測(cè),，來預(yù)測(cè)這些細(xì)菌的進(jìn)化機(jī)制以及給公眾的健康提供合理的建議，相關(guān)研究成果已于近日刊登在了國(guó)際雜志PloS Pathogen上,。
盡管病原菌可以利用多種途徑,、機(jī)制來感染人體的細(xì)胞，但是兩個(gè)小組的研究者發(fā)現(xiàn)了細(xì)菌感染機(jī)制共同的方式,，研究者們查閱了48種病原菌的相關(guān)感染機(jī)制,，以及他們的運(yùn)動(dòng)性、生長(zhǎng)比率,、和免疫細(xì)胞之間的作用方式等等,，最終研究者們得出了一個(gè)值ID50,，即在50%感染的細(xì)胞中能夠引起感染的最小的細(xì)菌細(xì)胞的數(shù)量。
研究小組發(fā)現(xiàn),，細(xì)菌細(xì)胞的ID需要達(dá)到250左右才能完全的摧毀吞噬細(xì)胞,，盡管細(xì)菌的ID50達(dá)到3000萬的時(shí)候，引發(fā)傳染的概率也微乎其微,，細(xì)菌在機(jī)體內(nèi)的感染需要不斷生長(zhǎng)增殖,，通過細(xì)菌獨(dú)有的群體感應(yīng)系統(tǒng)來進(jìn)行交流。
文章的第一作者Joao Gama表示,，在機(jī)體免疫系統(tǒng)和促使疾病的細(xì)菌之間,，有些細(xì)菌通過正面來攻擊免疫細(xì)胞，而有些細(xì)菌則秘密地搞地下活動(dòng),，來襲擊宿主的免疫系統(tǒng),，很多時(shí)候，細(xì)菌都是一會(huì)正面攻擊,，一會(huì)秘密攻擊宿主細(xì)胞的,，我們的研究發(fā)現(xiàn)，低的ID50表明細(xì)菌是秘密攻擊免疫細(xì)胞的,，而高的ID50則表明細(xì)菌是通過正面來對(duì)細(xì)胞進(jìn)行攻擊的,。（生物谷：T.Shen編譯）
doi:10.1371/journal.ppat.1002503
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Immune Subversion and Quorum-Sensing Shape the Variation in Infectious Dose among Bacterial Pathogens
João Alves Gama1,2, Sophie S. Abby3,4, Sara Vieira-Silva3,4, Francisco Dionisio1,2, Eduardo P. C. Rocha3,4*
Many studies have been devoted to understand the mechanisms used by pathogenic bacteria to exploit human hosts. These mechanisms are very diverse in the detail, but share commonalities whose quantification should enlighten the evolution of virulence from both a molecular and an ecological perspective. We mined the literature for experimental data on infectious dose of bacterial pathogens in humans (ID50) and also for traits with which ID50 might be associated. These compilations were checked and complemented with genome analyses. We observed that ID50 varies in a continuous way by over 10 orders of magnitude. Low ID50 values are very strongly associated with the capacity of the bacteria to kill professional phagocytes or to survive in the intracellular milieu of these cells. Inversely, high ID50 values are associated with motile and fast-growing bacteria that use quorum-sensing based regulation of virulence factors expression. Infectious dose is not associated with genome size and shows insignificant phylogenetic inertia, in line with frequent virulence shifts associated with the horizontal gene transfer of a small number of virulence factors. Contrary to previous proposals, infectious dose shows little dependence on contact-dependent secretion systems and on the natural route of exposure. When all variables are combined, immune subversion and quorum-sensing are sufficient to explain two thirds of the variance in infectious dose. Our results show the key role of immune subversion in effective human infection by small bacterial populations. They also suggest that cooperative processes might be important for successful infection by bacteria with high ID50. Our results suggest that trade-offs between selection for population growth-related traits and selection for the ability to subvert the immune system shape bacterial infectiousness. Understanding these trade-offs provides guidelines to study the evolution of virulence and in particular the micro-evolutionary paths of emerging pathogens.
