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Infection and Immunity, June 2003, p. 3000-3009, Vol. 71, No. 6
0019-9567/03/$08.00+0 DOI: 10.1128/IAI.71.6.3000-3009.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
Ruben Zamora,2 Matthew J. Lieber,1 Patricia C. Dos Santos,1 Tina M. L. Peterson,1 Nicole Emmith,1 Junghwa Lim,1 David A. Wink,3 and Yoram Vodovotz2
Department of Biochemistry, Virginia Tech, Blacksburg, Virginia 24061,1 Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania 15260,2 Radiation Biology Branch, National Cancer Institute, Bethesda, Maryland 208923
Received 7 January 2003/ Returned for modification 15 February 2003/ Accepted 12 March 2003
During the process of bloodfeeding by Anopheles stephensi, mammalian latent transforming growth factor ß1 (TGF-ß1) 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-ß1 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-ß1, TGF-ß1 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.
Present address: CRC for Diagnostics, School of Life Sciences, Queensland University of Technology, Brisbane 4002, Australia.
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