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1 Department of Medicine, Rhode Island Hospital and Brown University, Providence, RI, USA
2 Division of Gastroenterology, University of Cleveland, Case Western Reserve University, Cleveland, OH, USA
* To whom correspondence should be addressed. E-mail: Karen_Harnett{at}Brown.edu.
Cholinergic mechanisms are largely responsible for esophageal contraction in
response to swallowing or to in vitro electrical field stimulation (EFS). After induction of
experimental esophagitis by repeated acid perfusion, the responses to swallowing and to
EFS were significantly reduced, but contraction in response to ACh was not affected,
suggesting that cholinergic mechanisms are damaged by acid perfusion but myogenic
mechanisms are not. Measurements of ACh release in response to EFS confirmed that
release of ACh was reduced in esophagitis, when compared to normal controls.
To examine factors contributing to this neurophathy, normal esophageal strips were
incubated for 1-2 hours with the pro-inflammatory cytokines IL-1
(100u/ml), IL-6 (1
ng/ml), or tumor necrosis factor 
(TNF-) (1 ng/ml).
IL-1 and IL-6 levels, measured by western blot analysis, increased in esophagitis,
when compared to normal circular muscle. IL-1 and IL-6 reduced contraction in
response to EFS (2-10 Hz, 0.2 ms) but did not affect ACh-induced contraction,
suggesting that these cytokines inhibit ACh release, without affecting myogenic
contractile mechanisms. EFS-induced ACH release was significantly reduced in normal
esophageal strips by incubation in IL-1 or IL-6, suggesting that they may contribute to
the contractility changes.
TNF- at 1 ng/ml, however, did not affect the response to ACh or to electrical
stimulation, but inhibited both at higher concentrations. TNF- levels were low in
normal muscle and did not increase with esophagitis.
The data suggest that the pro-inflammatory cytokines IL-1 and IL-6 contribute
to reduced esophageal contraction by inhibiting release of ACh from myenteric neurons.
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