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Published on: June 25, 2012
Mast cell-mediated changes in smooth muscle contractility during mouse giardiasis
Erqiu Li1, Aiping Zhao, Terez Shea-Donohue
1Department of Biology, Reiss Building, Room 406, Georgetown University, Washington, DC 20057, USA.
Infection and Immunity
|July 11, 2007
Summary
Giardia intestinalis infection alters gastrointestinal transit by increasing smooth muscle contractions, mediated by mast cells and cholecystokinin (CCK). This response aids in parasite elimination.
Area of Science:
- Gastroenterology
- Immunology
- Parasitology
Background:
- Giardia intestinalis causes global diarrheal disease.
- Infections impact gastrointestinal transit via adaptive immunity and neuronal nitric oxide synthase.
- Nitric oxide acts as an inhibitory neurotransmitter, prompting investigation into excitatory pathways.
Purpose of the Study:
- To investigate excitatory pathways involved in the host response to Giardia infection.
- To understand the role of smooth muscle function changes in Giardia infections.
Main Methods:
- Infection of animal models with Giardia intestinalis.
- Measurement of longitudinal smooth muscle contractions in response to various stimuli (CCK, acetylcholine, etc.).
- Assessment of mast cell involvement using mast cell stabilizers (ketotifen, compound 48/80).
Main Results:
- Giardia infection increased spontaneous and cholecystokinin (CCK)-induced longitudinal smooth muscle contractions.
- Acetylcholine, 5-hydroxytryptamine, or peptide TFFLR did not elicit enhanced contractile responses.
- Mast cell depletion or inhibition blocked Giardia-induced smooth muscle contractions, implicating mast cells.
Conclusions:
- Giardia infection enhances smooth muscle contractility primarily through a CCK-mediated pathway involving mast cells.
- CCK release triggers mast cell degranulation, increasing smooth muscle contractility.
- These contractions, alongside nitric oxide-mediated relaxation, facilitate intestinal transit and parasite expulsion.
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