Wolbachia stimulates immune gene expression and inhibits plasmodium development in Anopheles gambiae.
Wolbachia stimulates immune gene expression and inhibits plasmodium development in Anopheles gambiae.
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DOI：
10.1371/journal.ppat.1001143
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发表时间：
2010-10-07
期刊：
影响因子：
6.7
通讯作者：
Sinkins SP
中科院分区：
文献类型：
--
作者：
Kambris Z;Blagborough AM;Pinto SB;Blagrove MS;Godfray HC;Sinden RE;Sinkins SP
内共生沃尔巴克氏菌的过度复制 wMelPop 菌株最近被证明能够诱导埃及伊蚊的免疫上调和抑制病原体传播。为了检查在疟疾媒介冈比亚按蚊中是否会出现类似的效果，通过胸腔内接种产生了 wMelPop 的短暂体细胞感染。与对照组相比，观察到六个选定免疫基因的上调，其中至少两个（LRIM1 和 TEP1）影响疟疾寄生虫的发育。稳定感染的An.冈比亚细胞系也显示出疟疾相关免疫基因的表达增加。在 wMelPop 感染队列中观察到疟原虫感染强度显着降低，并且通过基因敲除，获得了 TEP1 在该表型中作用的证据。比较伊蚊体细胞感染和稳定遗传性 wMelPop 感染的上调水平。埃及伊蚊显示，体细胞感染中的上调水平低于稳定转感染系中的水平；然而，在体细胞 wMelPop 感染的雌性中观察到丝虫线虫的发育受到抑制。因此，我们认为在 An 中观察到的效果。如果能够产生稳定遗传的 wMelPop 转染，并且沃尔巴克氏体的体细胞感染为检查对病原体发展或传播的影响提供了有用的模型，那么冈比亚的影响也可能更加明显。讨论了沃尔巴克氏体对疟疾媒介缩短寿命和直接抑制疟原虫发育能力的比较影响的数据。疟疾是世界上最具破坏性的疾病之一，特别是在非洲，迫切需要新的控制策略。在这里，我们发现沃尔巴克氏体细菌的存在抑制了非洲最重要的按蚊物种中疟疾寄生虫的发育。此外，我们还发现沃尔巴克氏体的存在会导致免疫基因的开启，这些基因已知会影响许多疟疾寄生虫物种的发育。再加上这种特定的沃尔巴克氏体菌株的寿命缩短效应，以及沃尔巴克氏体在昆虫种群中传播的一般能力，我们的研究为基于沃尔巴克氏体的疟疾控制方法的发展提供了刺激。它还为沃尔巴克氏体对昆虫的广泛影响提供了新的见解。
The over-replicating wMelPop strain of the endosymbiont Wolbachia pipientis has recently been shown to be capable of inducing immune upregulation and inhibition of pathogen transmission in Aedes aegypti mosquitoes. In order to examine whether comparable effects would be seen in the malaria vector Anopheles gambiae, transient somatic infections of wMelPop were created by intrathoracic inoculation. Upregulation of six selected immune genes was observed compared to controls, at least two of which (LRIM1 and TEP1) influence the development of malaria parasites. A stably infected An. gambiae cell line also showed increased expression of malaria-related immune genes. Highly significant reductions in Plasmodium infection intensity were observed in the wMelPop-infected cohort, and using gene knockdown, evidence for the role of TEP1 in this phenotype was obtained. Comparing the levels of upregulation in somatic and stably inherited wMelPop infections in Ae. aegypti revealed that levels of upregulation were lower in the somatic infections than in the stably transinfected line; inhibition of development of Brugia filarial nematodes was nevertheless observed in the somatic wMelPop infected females. Thus we consider that the effects observed in An. gambiae are also likely to be more pronounced if stably inherited wMelPop transinfections can be created, and that somatic infections of Wolbachia provide a useful model for examining effects on pathogen development or dissemination. The data are discussed with respect to the comparative effects on malaria vectorial capacity of life shortening and direct inhibition of Plasmodium development that can be produced by Wolbachia. Malaria is one of the world's most devastating diseases, particularly in Africa, and new control strategies are desperately needed. Here we show that the presence of Wolbachia bacteria inhibits the development of a malaria parasite in the most important Anopheles mosquito species of Africa. In addition we show that the presence of Wolbachia results in the switching on of immune genes that are known to affect development of many species of malaria parasite. When added to the lifespan-shortening effects of this particular strain of Wolbachia, and the general ability of Wolbachia to spread through insect populations, our study provides a stimulus for the development of Wolbachia-based malaria control methods. It also provides new insights into the wide range of effects of Wolbachia in insects.
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影响因子：
32.4
作者：
Frolet, Cecile;Thoma, Martine;Levashina, Elena A.
通讯作者：
Levashina, Elena A.
DOI：
10.1126/science.1175241
发表时间：
2009-10-02
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Blandin SA;Wang-Sattler R;Lamacchia M;Gagneur J;Lycett G;Ning Y;Levashina EA;Steinmetz LM
通讯作者：
Steinmetz LM
DOI：
10.1073/pnas.0504950102
发表时间：
2005-08-09
影响因子：
11.1
作者：
Meister, S;Kanzok, SM;Zheng, LB
通讯作者：
Zheng, LB
影响因子：
3.1
作者：
GWADZ, RW;KASLOW, D;MILLER, LH
通讯作者：
MILLER, LH
DOI：
10.1073/pnas.94.20.10792
发表时间：
1997-09-30
影响因子：
11.1
作者：
Min, KT;Benzer, S
通讯作者：
Benzer, S