Haemocytes respond to
infection by phagocytosing pathogens, producing the
enzymes that drive the
phenoloxidase-based melanization cascade, secreting lytic factors, and producing other humoral
proteins. A subset of haemocytes, called periostial haemocytes, aggregate on the surface of the heart of mosquitoes and kill pathogens in areas of high haemolymph flow. Periostial haemocytes are always present, but an
infection induces the recruitment of additional haemocytes to these regions. Here, we tested whether members of the
Nimrod gene family are involved in the periostial immune response of the African
malaria mosquito, Anopheles gambiae. Using organismal manipulations, RNA interference (RNAi) and microscopy, we show that, following an
infection with Escherichia coli,
nimrod - the orthologue of Drosophila NimB2 - is not involved in periostial responses. At 4 h postinfection, however, RNAi-based knockdown of draper results in a marginal increase in the number of periostial haemocytes and a doubling of E. coli accumulation at the periostial regions. Finally, at 24 h postinfection, knockdown of eater decreases the number of periostial haemocytes and decreases the phagocytosis of E. coli on the surface of the heart. Phagocytosis of bacteria is more prevalent in the periostial regions of the mid abdominal segments, and knockdown of draper,
nimrod or eater does not alter this distribution. Finally, knockdown of
Nimrod family genes did not have a meaningful effect on the accumulation of
melanin at the periostial regions. This study identifies roles for eater and draper in the functional integration of the mosquito immune and circulatory systems.