Project description:Transmission of malaria is dependent on the successful completion of the Plasmodium lifecycle in the Anopheles vector. Major obstacles are encountered in the midgut tissue, where most parasites are killed by the mosquito’s immune system. In the present study, DNA microarray analyses have been used to compare Anopheles gambiae responses to invasion of the midgut epithelium by the ookinete stage of the human pathogen Plasmodium falciparum and the rodent experimental model pathogen P. berghei. Invasion by P. berghei had a more profound impact on the mosquito transcriptome, including a variety of functional gene classes, while P. falciparum elicited a broader immune response at the gene transcript level. Ingestion of human malaria-infected blood lacking invasive ookinetes also induced a variety of immune genes, including several anti-Plasmodium factors. Keywords: Anopheles gambiae, Plasmodium falciparum, ookinete, invasion, innate immunity
Project description:Detoxification genes were assayed for their response to Plasmodium berghei infection at 1 and 11 days post infection in Anopheles gambiae mosquitoes.
Project description:Plasmodium ssp. are pathogens in their vertebrate hosts and also cause deleterious effects to their insect vectors. We show here, however, that Plasmodium-infected mosquitoes more efficiently accumulate energy resources (glycogen) during oocyst development, and survive better when they are starved. Microarray analysis revealed that mosquito metabolism is altered by the presence of rapidly growing oocysts in the midgut. Plasmodium infection is associated with enhanced expression of several insulin-like peptides in mosquitoes and blocking insulin-like signaling results in diminished Plasmodium development. We conclude that Plasmodium infection dramatically changes mosquito metabolism pathways, epitomized by enhanced insulin-signaling, and thereby confer a survival advantage to the insects during periods of starvation. Manipulation of this pathway may provide new strategies to influence the ability of mosquitoes to transmit the protozoa that cause malaria. One-condition experiment: P. berghei infected vs uninfected mosquitoes; 10 mosquitoes per sample; 4 biological replicates for each group; two different time points, 10 and 17 days post infection; control mosquitoes were from same batch as infected mosquitoes that were fed on clean mice.
Project description:Transmission of malaria is dependent on the successful completion of the Plasmodium lifecycle in the Anopheles vector. Major obstacles are encountered in the midgut tissue, where most parasites are killed by the mosquito’s immune system. In the present study, DNA microarray analyses have been used to compare Anopheles gambiae responses to invasion of the midgut epithelium by the ookinete stage of the human pathogen Plasmodium falciparum and the rodent experimental model pathogen P. berghei. Invasion by P. berghei had a more profound impact on the mosquito transcriptome, including a variety of functional gene classes, while P. falciparum elicited a broader immune response at the gene transcript level. Ingestion of human malaria-infected blood lacking invasive ookinetes also induced a variety of immune genes, including several anti-Plasmodium factors. By comparing gene expression patterns between carcassess or guts of mosquitoes that fed on a P. falciparum or P. berghei wt and mosquitoes that fed on invasion incapable strains we gain information on the A. gambiae transcriptional responses to the invading ookinete at 24 hours after feeding. By comparing gene expression patterns between carcassess or guts of mosquitoes that fed on a P. falciparum ookinete invasion incapable strain and mosquitoes that fed on non-infected blood we gain information on the A. gambiae transcriptional responses to malaria infected blood in absence of ookinete invasion at 24 hours after feeding. By comparing gene expression patterns between mosquitoes at 4 hours after being injected with either E. coli or S. aureus and mosquitoes injected with sterile PBS we gain information on the mosquito's transcriptional response to these bacterial challenges.
Project description:Insect hemocytes mediate important cellular immune responses including phagocytosis and encapsulation, and also secrete immune factors such as opsonins, melanization factors, and antimicrobial peptides. In Anopheles, they contribute to the defense against malaria parasite invasion during the early sporogonic cycle. We used microarrays to identify if and to what degree circulating hemocytes have altered global expression profiles after infection with the rodent malaria parasite, Plasmodium berghei
Project description:Salivary glands are the only mosquito tissue invaded by Plasmodium sporozoites being a key stage for the effective parasite transmission and maturation, making knowledge regarding Anopheles sialome highly relevant to understand this process. In this study, we report for the first time a transcriptomic analysis using RNA-seq of An. gambiae infected by P. berghei.
Project description:Proteomic analysis of Anopheles gambiae brain tissue after in-gel trypsin digestion. To gain insights into neurobiology of the Anopheles gambiae mosquito, we carried out a proteomic analysis of its brain using a comprehensive proteomic approach.
Project description:Plasmodium ssp. are pathogens in their vertebrate hosts and also cause deleterious effects to their insect vectors. We show here, however, that Plasmodium-infected mosquitoes more efficiently accumulate energy resources (glycogen) during oocyst development, and survive better when they are starved. Microarray analysis revealed that mosquito metabolism is altered by the presence of rapidly growing oocysts in the midgut. Plasmodium infection is associated with enhanced expression of several insulin-like peptides in mosquitoes and blocking insulin-like signaling results in diminished Plasmodium development. We conclude that Plasmodium infection dramatically changes mosquito metabolism pathways, epitomized by enhanced insulin-signaling, and thereby confer a survival advantage to the insects during periods of starvation. Manipulation of this pathway may provide new strategies to influence the ability of mosquitoes to transmit the protozoa that cause malaria.