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Malaria-transmitting mosquitoes are continuously exposed to microbes, including their midgut microbiota. This naturally acquired microbial flora can modulate the mosquito's vectorial capacity by inhibiting the development of  Plasmodium  and other human pathogens through an unknown mechanism. We have undertaken a comprehensive functional genomic approach to elucidate the molecular interplay between the bacterial co-infection and the development of the human malaria parasite  Plasmodium falciparum  in its natural vector  Anopheles gambiae . Global transcription profiling of septic and aseptic mosquitoes identified a significant subset of immune genes that were mostly up-regulated by the mosquito's microbial flora, including several anti- Plasmodium  factors. Microbe-free aseptic mosquitoes displayed an increased susceptibility to  Plasmodium  infection while co-feeding mosquitoes with bacteria and  P. falciparum  gametocytes resulted in lower than normal infection levels. Infection analyses suggest the bacteria-mediated anti- Plasmodium  effect is mediated by the mosquitoes' antimicrobial immune responses, plausibly through activation of basal immunity. We show that the microbiota can modulate the anti- Plasmodium  effects of some immune genes. In sum, the microbiota plays an essential role in modulating the mosquito's capacity to sustain  Plasmodium  infection.

Implication of the Mosquito Midgut Microbiota in the Defense against Malaria Parasites