Mammalian transforming growth factor beta1 activated after ingestion by Anopheles stephensi modulates mosquito immunity

During the process of bloodfeeding by Anopheles stephensi, mammalian latent transforming growth factor beta1 (TGF-beta1) 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...

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Bibliographic Details
Published in:Infection and immunity 2003-06, Vol.71 (6), p.3000-3009
Main Authors: Luckhart, Shirley, Crampton, Andrea L, Zamora, Ruben, Lieber, Matthew J, Dos Santos, Patricia C, Peterson, Tina M L, Emmith, Nicole, Lim, Junghwa, Wink, David A, Vodovotz, Yoram
Format: Article
Language:English
Subjects:
Animals
Anopheles - immunology
Anopheles - parasitology
Humans
Intestinal Mucosa - metabolism
Malaria - transmission
Nitric Oxide - biosynthesis
Nitric Oxide Synthase - biosynthesis
Penicillamine - analogs & derivatives
Penicillamine - pharmacology
Peroxynitrous Acid - pharmacology
Plasmodium falciparum - growth & development
Transforming Growth Factor beta - physiology
Transforming Growth Factor beta1
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Summary:During the process of bloodfeeding by Anopheles stephensi, mammalian latent transforming growth factor beta1 (TGF-beta1) 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-beta1 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-beta1, TGF-beta1 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.
ISSN:0019-9567