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Department of Physiology and Cell Biology, Ohio State University, College of Medicine and Public Health, Columbus, Ohio 43210
Enteric neuroimmune interactions in
gastrointestinal hypersensitivity responses involve antigen detection
by mast cells, mast cell degranulation, release of chemical mediators,
and modulatory actions of the mediators on the enteric nervous system
(ENS). Electrophysiological methods were used to investigate electrical and synaptic behavior of neurons in the stomach and small intestine during exposure to 
-lactoglobulin in guinea pigs sensitized to cow's milk. Application of -lactoglobulin to sensitized
preparations depolarized the membrane potential and increased neuronal
excitability in small intestinal neurons but not in gastric neurons.
Effects on membrane potential and excitability in the small intestine were suppressed by the mast cell stabilizing drug ketotifen, the histamine H2 receptor antagonist cimetidine, the
cyclooxygenase inhibitor piroxicam, and the 5-lipoxygenase inhibitor
caffeic acid. Unlike small intestinal ganglion cells, gastric myenteric neurons did not respond to histamine applied exogenously. Antigenic exposure suppressed noradrenergic inhibitory neurotransmission in the
small intestinal submucosal plexus. The histamine H3
receptor antagonist thioperamide and piroxicam, but not caffeic acid,
prevented the allergic suppression of noradrenergic inhibitory
neurotransmission. Antigenic stimulation of neuronal excitability and
suppression of synaptic transmission occurred only in milk-sensitized
animals. Results suggest that signaling between mast cells and the ENS underlies intestinal, but not gastric, anaphylactic responses associated with food allergies. Histamine, prostaglandins, and leukotrienes are paracrine signals in the communication pathway from
mast cells to the small intestinal ENS.
food allergy; enteric nervous system; enteric immune system; anaphylaxis; mast cells
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