A Gut Symbiotic Bacterium Serratia marcescens Renders Mosquito Resistance to Plasmodium Infection Through Activation of Mosquito Immune Responses
A Gut Symbiotic Bacterium Serratia marcescens Renders Mosquito Resistance to Plasmodium Infection Through Activation of Mosquito Immune Responses
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肠道共生细菌粘质沙雷氏菌通过激活蚊子免疫反应使蚊子对疟原虫感染产生抵抗力
DOI：
10.3389/fmicb.2019.01580
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发表时间：
2019-07-18
影响因子：
5.2
通讯作者：
Wang, Sibao
中科院分区：
文献类型：
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作者：
Bai, Liang;Wang, Lili;Wang, Sibao
疟疾在蚊子中肠的发展是一个复杂的过程，会导致相当大的寄生虫损失。蚊子肠道微生物区系影响蚊子病原体感染的结果，但肠道共生菌影响媒介能力的潜在机制仍不清楚。在这里，我们从中国现场捕获的中华按蚊中分离到两株沙雷氏菌(Y1和J1)，并评价了它们对疟疾生长发育的影响。斯特芬西。安的殖民。沙雷氏菌Y1感染斯氏中肠能显著提高蚊虫对伯氏疟原虫感染的抵抗力，而沙雷氏菌J1对寄生虫的发育没有影响。沙雷氏菌Y1对寄生虫的抑制是通过激活蚊子免疫系统来诱导的。RNA-seq的全基因组转录分析显示，在喂糖的蚊子中，对沙雷氏菌Y1和J1的反应，中肠基因的表达模式类似。然而，在摄血后24小时，沙雷氏菌Y1比沙雷氏菌J1调节更多的中肠基因，包括c型凝集素(CTL)、Clip丝氨酸蛋白酶和其他免疫效应因子。此外，沉默沙雷氏菌Y1诱导的几种抗疟原虫因子，如硫酯蛋白1(TEP1)、纤维蛋白原免疫凝集素9(FBN9)或富含亮氨酸的重复蛋白LRRD7，可以在沙雷氏菌Y1存在的情况下挽救寄生虫卵囊的发育，提示这些因素调节了沙雷氏菌Y1介导的抗疟原虫作用。这项研究加深了我们对肠道细菌如何影响蚊子和疟原虫相互作用的理解。
The malaria development in the mosquito midgut is a complex process that results in considerable parasite losses. The mosquito gut microbiota influences the outcome of pathogen infection in mosquitoes, but the underlying mechanisms through which gut symbiotic bacteria affect vector competence remain elusive. Here, we identified two Serratia strains (Y1 and J1) isolated from field-caught female Anopheles sinensis from China and assessed their effect on Plasmodium development in An. stephensi. Colonization of An. stephensi midgut by Serratia Y1 significantly renders the mosquito resistant to Plasmodium berghei infection, while Serratia J1 has no impact on parasite development. Parasite inhibition by Serratia Y1 is induced by the activation of the mosquito immune system. Genome-wide transcriptomic analysis by RNA-seq shows a similar pattern of midgut gene expression in response to Serratia Y1 and J1 in sugar-fed mosquitoes. However, 24 h after blood ingestion, Serratia Y1 modulates more midgut genes than Serratia J1 including the c-type lectins (CTLs), CLIP serine proteases and other immune effectors. Furthermore, silencing of several Serratia Y1-induced anti-Plasmodium factors like the thioester-containing protein 1 (TEP1), fibrinogen immunolectin 9 (FBN9) or leucine-rich repeat protein LRRD7 can rescue parasite oocyst development in the presence of Serratia Y1, suggesting that these factors modulate the Serratia Y1-mediated anti-Plasmodium effect. This study enhances our understanding of how gut bacteria influence mosquito-Plasmodium interactions.