近日，國際著名雜志《美國國家科學(xué)院院刊》PNAS在線刊登了美國加利福尼亞大學(xué)研究人員的最新研究成果“Wolbachia induces reactive oxygen species (ROS)-dependent activation of the Toll pathway to control dengue virus in the mosquito Aedes aegypti,，”,，文章中，作者解釋了沃爾巴克氏體細(xì)菌通過激活活性氧依賴的Toll途徑來控制伊蚊體內(nèi)的登革熱病毒,。
登革熱是一種病毒引起的疾病,，主要發(fā)生在熱帶，全球每年大約有5000萬人受感染,。登革熱爆發(fā)的嚴(yán)重性在增強(qiáng),，涉及的地理范圍也在擴(kuò)大。能傳染登革熱的蚊子對能殺死它們的殺蟲劑也逐漸變得有抗藥性,。登革熱通常不會致人死亡,，但是它能讓患者病重。對于發(fā)展中國家人民來說這能造成嚴(yán)重的經(jīng)濟(jì)后果,。
沃爾巴克式體存活于細(xì)胞的細(xì)胞質(zhì)中,，通過母體排卵的方式一代代的繁衍。它造成細(xì)胞質(zhì)不相容,，給細(xì)菌提供一種強(qiáng)大的機(jī)制侵入昆蟲群體,。受感染的母體既可以和受感染的雄性也可以和沒有受感染的雄性交配，但是未受感染的雌性只能和未受感染的雄性成功交配,。如果未受感染的雌性和受感染的雄性交配,，它的后代會死亡。這意味著受感染的雌性具有選擇上的優(yōu)勢,，因?yàn)樗鼈冊谶x擇雄性時有更大的選擇范圍,。
文章中，作者闡述了沃爾巴克式體細(xì)菌是如何對登革熱病毒產(chǎn)生抗性進(jìn)而影響伊蚊的,，作者用沃爾巴克式體感染伊蚊后,，進(jìn)行了微陣列實(shí)驗(yàn)，發(fā)現(xiàn)伊蚊體內(nèi)與免疫和氧化還原反應(yīng)相關(guān)的基因的轉(zhuǎn)錄表達(dá)量都升高了,，細(xì)菌的感染可以誘導(dǎo)文字體內(nèi)的氧化應(yīng)激性以及活性氧水平的升高,，活性氧的水平和Toll途徑的激活直接相關(guān)，而Toll途徑直接介導(dǎo)抗氧化劑的表達(dá)用來應(yīng)對氧化壓力,，這種免疫途徑對抗微生物多肽（如防御素類或者蛾血素）的激活也是極其相關(guān)的,，作者目前的證據(jù)顯示，抗微生物多肽在含沃爾巴克式體的蚊子中可以抑制登革熱病毒的繁殖,，目前利用轉(zhuǎn)基因蚊子和RNAi的方法可以達(dá)到同樣的目的,，就是在含沃爾巴克式體的蚊子中可以抑制登革熱病毒的增殖,。
研究者進(jìn)行了一系列的實(shí)驗(yàn)，最后發(fā)現(xiàn)了共生細(xì)菌可以利用宿主的免疫系統(tǒng)來促進(jìn)自己在宿主內(nèi)的持續(xù)感染,，最終在有登革熱病毒的蚊子體內(nèi)持續(xù)生存,，最終使帶有病毒的蚊子死亡，遏制登革熱病毒的傳播,，作者的研究發(fā)現(xiàn)將會給抑制蚊子疾病的傳播帶來非常大的幫助和支持,。（生物谷Bioon.com）
（T.Shen編譯 如有問題請及時指正）
doi:10.1073/pnas.1116932108
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Wolbachia induces reactive oxygen species (ROS)-dependent activation of the Toll pathway to control dengue virus in the mosquito Aedes aegypti
Xiaoling Pana, Guoli Zhoua, Jiahong Wua,b, Guowu Biana,c, Peng Lua, Alexander S. Raikheld,e,1, and Zhiyong Xia,c,1
Wolbachia are maternally transmitted symbiotic bacteria that can spread within insect populations because of their unique ability to manipulate host reproduction. When introduced to nonnative mosquito hosts, Wolbachia induce resistance to a number of human pathogens, including dengue virus (DENV), Plasmodium, and filarial nematodes, but the molecular mechanism involved is unclear. In this study, we have deciphered how Wolbachia infection affects the Aedes aegypti host in inducing resistance to DENV. The microarray assay indicates that transcripts of genes with functions related to immunity and reduction-oxidation (redox) reactions are up-regulated in Ae. aegypti infected with Wolbachia. Infection with this bacterium leads to induction of oxidative stress and an increased level of reactive oxygen species in its mosquito host. Reactive oxygen species elevation is linked to the activation of the Toll pathway, which is essential in mediating the expression of antioxidants to counterbalance oxidative stress. This immune pathway also is responsible for activation of antimicrobial peptides—defensins and cecropins. We provide evidence that these antimicrobial peptides are involved in inhibition of DENV proliferation in Wolbachia-infected mosquitoes. Utilization of transgenic Ae. aegypti and the RNAi depletion approach has been instrumental in proving the role of defensins and cecropins in the resistance of Wolbachia-infected Ae. aegypti to DENV. These results indicate that a symbiotic bacterium can manipulate the host defense system to facilitate its own persistent infection, resulting in a compromise of the mosquito's ability to host human pathogens. Our discoveries will aid in the development of control strategies for mosquito-transmitted diseases.
