TY - JOUR
T1 - Natural microbe-mediated refractoriness to Plasmodium infection in Anopheles gambiae
AU - Cirimotich, Chris M.
AU - Dong, Yuemei
AU - Clayton, April M.
AU - Sandiford, Simone L.
AU - Souza-Neto, Jayme A.
AU - Mulenga, Musapa
AU - Dimopoulos, George
PY - 2011/5/13
Y1 - 2011/5/13
N2 - Malaria parasite transmission depends on the successful transition of Plasmodium through discrete developmental stages in the lumen of the mosquito midgut. Like the human intestinal tract, the mosquito midgut contains a diverse microbial flora, which may compromise the ability of Plasmodium to establish infection. We have identified an Enterobacter bacterium isolated from wild mosquito populations in Zambia that renders the mosquito resistant to infection with the human malaria parasite Plasmodium falciparum by interfering with parasite development before invasion of themidgut epithelium. Phenotypic analyses showed that the anti-Plasmodium mechanism requires small populations of replicating bacteria and is mediated through a mosquito-independent interaction with the malaria parasite. We show that this anti-Plasmodium effect is largely caused by bacterial generation of reactive oxygen species.
AB - Malaria parasite transmission depends on the successful transition of Plasmodium through discrete developmental stages in the lumen of the mosquito midgut. Like the human intestinal tract, the mosquito midgut contains a diverse microbial flora, which may compromise the ability of Plasmodium to establish infection. We have identified an Enterobacter bacterium isolated from wild mosquito populations in Zambia that renders the mosquito resistant to infection with the human malaria parasite Plasmodium falciparum by interfering with parasite development before invasion of themidgut epithelium. Phenotypic analyses showed that the anti-Plasmodium mechanism requires small populations of replicating bacteria and is mediated through a mosquito-independent interaction with the malaria parasite. We show that this anti-Plasmodium effect is largely caused by bacterial generation of reactive oxygen species.
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U2 - 10.1126/science.1201618
DO - 10.1126/science.1201618
M3 - Article
C2 - 21566196
AN - SCOPUS:79956047791
SN - 0036-8075
VL - 332
SP - 855
EP - 858
JO - Science
JF - Science
IS - 6031
ER -