uChE, butyrylcholinesterase

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Nippostrongylus Brasiliensis: Infection Induces Upregulation of Acetylcholinesterase Activity on Rat Intestinal Epithelial Cells

Journal Title, Volume, Page: 
Experimental Parasitology, Volume:96, Issue:4, December 2000, Pages:222-230
Year of Publication: 
2000
Authors: 
Ayman S Hussein
Department of Biochemistry, Imperial College of Science, Technology and Medicine, London, SW7 2AY, United Kingdom
Current Affiliation: 
Faculty of Medicine & Health Sciences, Department of Biomedical Sciences, An-Najah National University, Nablus, Palestine
Wayne S Russell
Department of Biochemistry, Imperial College of Science, Technology and Medicine, London, SW7 2AY, United Kingdom
Siân M Henson
Department of Biochemistry, Imperial College of Science, Technology and Medicine, London, SW7 2AY, United Kingdom
John R Tippins
Department of Biochemistry, Imperial College of Science, Technology and Medicine, London, SW7 2AY, United Kingdom
Murray E Selkirk
Department of Biochemistry, Imperial College of Science, Technology and Medicine, London, SW7 2AY, United Kingdom
Preferred Abstract (Original): 

Expression Of Cholines Terases And Muscarinic Acetylcholine Receptors In The Jejunal Mucosa Has Been Investigated During Infection Of Rats With The Nematode Parasite NippostrongylusBrasiliensis. Selective Expression Of M3 Receptors Was Observed On Epithelial Cells From Uninfected Rats And Animals 7 Days Postinfection, And Saturation Binding With [3H]Quinuclidinyl Benzilate Indicated That Receptor Expression On Cell Membranes Was Unaltered By Infection. Butyrylcholinesterase Was Highly Expressed In Mucosal Epithelia, But Acetylcholinesterase Was Present At Low Levels In Unin Fected Animals. In Contrast, Discrete Foci Of Intense Acetylcholinesterase Activity Were Observed On The Basement Membrane Of Intestinal Epithelial Cells In Animals Infected With N. Brasiliensis. This Was Demonstrated To Be Due To Upregulation Of Expression Of Endogenous Enzyme, Which Peaked At Day 10 Postinfection And Subsequently Declined To Preinfection Levels. It Is Suggested That This Occurs In Response To Hyper-Activation Of The Enteric Nervous System As A Result Of Infection, And May Benefit The Host By Limiting Excessive Fluid Secretion Due To Cholinergic Stimulation.

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