The Anopheles FBN9 immune factor mediates Plasmodium species-specific defense through transgenic fat body expression.
Mosquitoes have a multifaceted innate immune system that is actively engaged in warding off various pathogens, including the protozoan malaria parasite Plasmodium. Various immune signaling pathways and effectors have been shown to mediate a certain degree of defense specificity against different Plasmodium species. A key pattern recognition receptor of the Anopheles gambiae immune system is the fibrinogen domain-containing immunolectin FBN9, which has been shown to be transcriptonally induced by Plasmodium infection, and to mediate defense against both rodent and human malaria parasites and bacteria. Here we have further studied the defense specificity of FBN9 using a transgenic approach, in which FBN9 is overexpressed in the fat body tissue after a blood meal through a vitellogenin promoter. Interestingly, the Vg-FBN9 transgenic mosquitoes showed increased resistance only to the rodent parasite P. berghei, and not to the human parasite P. falciparum, pointing to differences in the mosquito's defense mechanisms against the two parasite species. The Vg-FBN9 transgenic mosquitoes were also more resistant to infection with both Gram-positive and Gram-negative bacteria and showed increased longevity when infected with P. berghei. Our study points to the importance of both experimentally depleting and enriching candidate anti-Plasmodium effectors in functional studies in order to ascertain their suitability for the development of transgenic mosquito-based malaria control strategies.
W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, 615 N. Wolfe St., Baltimore, MD 21205, USA.
Maria L
ML
Simões
W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, 615 N. Wolfe St., Baltimore, MD 21205, USA.
Yuemei
Y
Dong
Department of Life Sciences, Imperial College London, SW7 2AZ, UK.
Andrew
A
Hammond
Department of Life Sciences, Imperial College London, SW7 2AZ, UK.
Ann
A
Hall
Department of Life Sciences, Imperial College London, SW7 2AZ, UK.
Andrea
A
Crisanti
Department of Life Sciences, Imperial College London, SW7 2AZ, UK.
Tony
T
Nolan
W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, 615 N. Wolfe St., Baltimore, MD 21205, USA. Electronic address: gdimopo@jhu.edu.
George
G
Dimopoulos
D000818:Animals; D030801:Animals, Genetically Modified; D000852:Anopheles / Q000276:immunology*; D002478:Cells, Cultured; D004926:Escherichia coli / Q000276:immunology*; D004927:Escherichia coli Infections / Q000276:immunology*; D005216:Fat Body / Q000502:physiology*; D005298:Fertility; D000071837:Fibrillins / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D007113:Immunity, Innate; D008288:Malaria / Q000276:immunology*; D010962:Plasmodium berghei / Q000276:immunology*; D010963:Plasmodium falciparum / Q000276:immunology*; D011401:Promoter Regions, Genetic / Q000235:genetics; D051192:Receptors, Pattern Recognition / Q000235:genetics / Q000378:metabolism*; D012377:Rodentia; D013045:Species Specificity; D013203:Staphylococcal Infections / Q000276:immunology*; D013211:Staphylococcus aureus / Q000276:immunology*; D019076:Transgenes / Q000235:genetics; D014819:Vitellogenins / Q000235:genetics
D000071837:Fibrillins; D051192:Receptors, Pattern Recognition; D014819:Vitellogenins
Anopheles gambiae; FBN9; Immunity; Plasmodium; Transgenesis