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Background  Malaria is a worldwide infectious disease caused by  Plasmodium  parasites and transmitted by female  Anopheles  mosquitoes. The malaria vector mosquito  Anopheles  can trigger effective mechanisms to control completion of the  Plasmodium  lifecycle; the mosquito immune response to the parasite involves several pathways which are not yet well characterized.  Plasmodium  metabolite hemozoin has emerged as a potent immunostimulator of mammalian tissues. In this study, we aim to investigate the role of this parasite’s by-product as stimulator of  Anopheles gambiae  immunity to  Plasmodium berghei .    Methods  Female mosquitoes were inoculated with hemozoin and the  Plasmodium  infection rate and intensity were measured. Differences between treatments were detected by Zero-inflated models. Microarray transcription analysis was performed to assess gene expression response to hemozoin. Genome-wide analysis results were confirmed by stimulation of  Anopheles gambiae  tissues and cells with hemozoin and silencing of REL2-F and its negative regulator Caspar.    Results  Gene expression profiles revealed that hemozoin activates several immunity genes, including pattern recognition receptors (PRRs) and antimicrobial peptides (AMPs). Importantly, we found that the Immune deficiency (Imd) pathway Nuclear Factor-kappaB (NF-κB) transcription factor REL2, in its full-length form REL2-F, was induced upon hemozoin treatment.    Conclusions  We have for the first time shown the impact of hemozoin treatment in  Plasmodium  infection, reducing both rate and intensity of the infection. We propose that hemozoin boosts the innate immunity in  Anopheles , activating key effector genes involved in mosquito resistance to  Plasmodium,  and this activation is REL2-mediated.    Electronic supplementary material  The online version of this article (doi:10.1186/s13071-014-0619-y) contains supplementary material, which is available to authorized users.

Hemozoin activates the innate immune system and reduces Plasmodium berghei infection in Anopheles gambiae