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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.

A Gut Symbiotic Bacterium Serratia marcescens Renders Mosquito Resistance to Plasmodium Infection Through Activation of Mosquito Immune Responses