Abstract
During the process of bloodfeeding by
Anopheles stephensi
, mammalian latent transforming growth factor β1 (TGF-β1) is ingested and activated rapidly in the mosquito midgut. Activation may involve heme and nitric oxide (NO), agents released in the midgut during blood digestion and catalysis of
l-
arginine oxidation by
A. stephensi
NO synthase (AsNOS). Active TGF-β1 persists in the mosquito midgut to extended times postingestion and is recognized by mosquito cells as a cytokine. In a manner analogous to the regulation of vertebrate inducible NO synthase and malaria parasite (
Plasmodium
) infection in mammals by TGF-β1, TGF-β1 regulates
AsNOS
expression and
Plasmodium
development in
A. stephensi
. Together, these observations indicate that, through conserved immunological cross talk, mammalian and mosquito immune systems interface with each other to influence the cycle of
Plasmodium
development.