Format

Send to

Choose Destination
See comment in PubMed Commons below
Dev Comp Immunol. 2012 Jul;37(3-4):390-401. doi: 10.1016/j.dci.2012.01.005. Epub 2012 Feb 2.

Increased survivorship following bacterial infection by the mosquito Aedes aegypti as compared to Anopheles gambiae correlates with increased transcriptional induction of antimicrobial peptides.

Author information

1
Department of Biological Sciences, Vanderbilt University, Nashville, TN 37235-1634, USA.

Abstract

Mosquitoes defend themselves from pathogens by mounting cellular and humoral innate immune responses. Bioinformatic analyses have revealed considerable divergence in immune gene repertoires between mosquito species, but interspecies empirical comparisons of immune responses are lacking. Here, we present a comparative analysis of the antimicrobial responses of two distantly related disease vectors: Aedes aegypti and Anopheles gambiae. Survival studies showed that Ae. aegypti are more proficient in surviving a bacterial infection than An. gambiae, and this correlates with Ae. aegypti's superior ability to kill bacteria in their hemocoels. Hemocytes from both species swiftly phagocytose bacteria, but phagocytosis does not explain Ae. aegypti's increased robustness: An. gambiae contain more circulating hemocytes and display a higher phagocytic index, but the phagocytic capacity of individual hemocytes is greater in Ae. aegypti. Then, profiling of 19 immunity genes revealed that transcriptional induction following infection is significantly elevated in Ae. aegypti when compared to An. gambiae, with the largest change seen in the transcription of cecropin and defensin. These data show that Ae. aegypti is better equipped to survive a bacterial infection than An. gambiae, and this correlates with Ae. aegypti's increased transcriptional induction of antimicrobial peptides and other humoral immune factors in response to infection.

PMID:
22326457
DOI:
10.1016/j.dci.2012.01.005
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center