blood feeding and insulin-like peptide 3 stimulate proliferation of hemocytes in the mosquito aedes aegypti血喂养和胰岛素样肽3刺激增殖通过姬氏的蚊子埃及伊蚊.pdfVIP

blood feeding and insulin-like peptide 3 stimulate proliferation of hemocytes in the mosquito aedes aegypti血喂养和胰岛素样肽3刺激增殖通过姬氏的蚊子埃及伊蚊.pdf

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blood feeding and insulin-like peptide 3 stimulate proliferation of hemocytes in the mosquito aedes aegypti血喂养和胰岛素样肽3刺激增殖通过姬氏的蚊子埃及伊蚊

Blood Feeding and Insulin-like Peptide 3 Stimulate Proliferation of Hemocytes in the Mosquito Aedes aegypti Julio Castillo1¤, Mark R. Brown1,2, Michael R. Strand 1,2* 1 Department of Entomology, University of Georgia, Athens, Georgia, United States of America, 2 Center for Tropical and Emerging Global Diseases, University of Georgia, Athens, Georgia, United States of America Abstract All vector mosquito species must feed on the blood of a vertebrate host to produce eggs. Multiple cycles of blood feeding also promote frequent contacts with hosts, which enhance the risk of exposure to infectious agents and disease transmission. Blood feeding triggers the release of insulin-like peptides (ILPs) from the brain of the mosquito Aedes aegypti, which regulate blood meal digestion and egg formation. In turn, hemocytes serve as the most important constitutive defense in mosquitoes against pathogens that enter the hemocoel. Prior studies indicated that blood feeding stimulates hemocytes to increase in abundance, but how this increase in abundance is regulated is unknown. Here, we determined that phagocytic granulocytes and oenocytoids express the A. aegypti insulin receptor (AaMIR). We then showed that: 1) decapitation of mosquitoes after blood feeding inhibited hemocyte proliferation, 2) a single dose of insulin-like peptide 3 (ILP3) sufficient to stimulate egg production rescued proliferation, and 3) knockdown of the AaMIR inhibited ILP3 rescue activity. Infection studies indicated that increased hemocyte abundance enhanced clearance of the bacterium Escherichia coli at lower levels of infection. Surprisingly, however, non-blood fed females better survived intermediate and high levels of E. coli infection than blood fed females. Taken together, our results reveal a previously unrecognized role for the insulin

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