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The alteration in signal transduction parameters induced by the excretory–secretory product from Giardia lamblia

Published online by Cambridge University Press:  14 September 2004

J. SHANT
Affiliation:
Department of Experimental Medicine and Biotechnology, PGIMER, Chandigarh, India.
S. GHOSH
Affiliation:
Department of Experimental Medicine and Biotechnology, PGIMER, Chandigarh, India.
S. BHATTACHARYYA
Affiliation:
Department of Experimental Medicine and Biotechnology, PGIMER, Chandigarh, India.
N. K. GANGULY
Affiliation:
Department of Experimental Medicine and Biotechnology, PGIMER, Chandigarh, India.
S. MAJUMDAR
Affiliation:
Department of Experimental Medicine and Biotechnology, PGIMER, Chandigarh, India.

Abstract

The mechanism by which Giardia lamblia exerts its pathogenicity is likely to be multifactorial. A 58 kDa enterotoxin was purified and characterized from the excretory–secretory product (ESP) of the parasite (Kaur et al. 2001). In the present study an attempt has been made to elucidate the mechanism of action of the ESP, a potentially important enterotoxin. A 41 kDa glycoprotein was identified in the mouse enterocyte membrane fraction with which the ESP interacted in a GM1-specific manner. The GTPase activity was reduced in enterocytes stimulated with the ESP, resulting in an increase in the level of adenylate cyclase-dependent cyclic adenosine monophosphate (cAMP). The activity of protein kinase A (PKA) in the enterocytes was also upregulated after ESP treatment. Ultimately, a significant increase in intracellular Ca2+ concentration and decrease in cytosolic Cl level were noticed in ESP-stimulated mouse enterocytes. Thus it is possible that the enterotoxic ESP could bind to the 41 kDa glycoprotein (receptor?) on the enterocytes and activate the G-protein-mediated signal transduction pathway resulting in alteration of electrolyte transport.

Type
Research Article
Copyright
2004 Cambridge University Press

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