Abstract
Exposure of Anopheles gambiae mosquitoes to Plasmodium infection enhances the ability of their immune system to respond to subsequent infections. However, the molecular mechanism that allows the insect innate immune system to ‘remember' a previous encounter with a pathogen has not been established. Challenged mosquitoes constitutively release a soluble haemocyte differentiation factor into their haemolymph that, when transferred into Naive mosquitoes, also induces priming. Here we show that this factor consists of a Lipoxin/Lipocalin complex. We demonstrate that innate immune priming in mosquitoes involves a persistent increase in expression of Evokin (a lipid carrier of the lipocalin family), and in their ability to convert arachidonic acid to lipoxins, predominantly Lipoxin A4. Plasmodium ookinete midgut invasion triggers immune priming by inducing the release of a mosquito lipoxin/lipocalin complex.
Highlights
Exposure of Anopheles gambiae mosquitoes to Plasmodium infection enhances the ability of their immune system to respond to subsequent infections
We describe the identification of haemocyte differentiation factor (HDF) as a Lipoxin/Lipocalin complex, and show that innate immune priming involves a persistent increase in the ability of mosquitoes to convert arachidonic acid to lipoxins, as well as higher expression of their lipid carrier, a member of the lipocalin family that we named Evokin
The stability and biochemical nature of HDF was explored using a bioassay in which haemolymph from Challenged mosquitoes was collected 5–7 days post infection and subjected to different treatments before it was injected into Naive recipients
Summary
Exposure of Anopheles gambiae mosquitoes to Plasmodium infection enhances the ability of their immune system to respond to subsequent infections. Pre-exposure of Anopheles gambiae mosquitoes to Plasmodium infection, in the presence of the gut microbiota, enhances the immune response to subsequent infections[2]. In both Drosophila[1] and mosquitoes[2], haemocytes have been shown to be essential for enhanced immunity after a challenge. We describe the identification of HDF as a Lipoxin/Lipocalin complex, and show that innate immune priming involves a persistent increase in the ability of mosquitoes to convert arachidonic acid to lipoxins, as well as higher expression of their lipid carrier, a member of the lipocalin family that we named Evokin
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