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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.
A soluble factor induced by Plasmodiuminfection promotes hemocyte differentiation and increases mosquitoe resistance to subsequent infections. Here the authors show that this factor consists of a Lipocalin/Lipoxin A4 complex, and that insects can metabolize arachidonic acid to produce lipoxins.
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Details
1 Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, USA (GRID:grid.48336.3a) (ISNI:0000 0004 1936 8075)
2 Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, USA (GRID:grid.48336.3a) (ISNI:0000 0004 1936 8075); Present address: Laboratório de Entomologia Médica, Centro de Pesquisas Rene Rachou—Fiocruz, Belo Horizonte, Brazil., (GRID:grid.418068.3) (ISNI:0000 0001 0723 0931)
3 Center for Experimental Therapeutics and Reperfusion Injury, Perioperative, and Pain Medicine, Brigham and Women’s Hospital and Harvard Medical School, Department of Anesthesiology, Boston, USA (GRID:grid.38142.3c) (ISNI:000000041936754X)