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Vol. 286, Issue 2, 657-661, August 1998
Department of Medicine I, University of Ulm, Germany (M.R., G.F.,
S.E., I.G., G.A),
Division of Gastroenterology, Harbor-UCLA Medical
Center, Torrance, CA (V.E.E.), and
Center for Ulcer Research and
Education (CURE), Los Angeles, CA (H.W., J.H.W.)
Recently we demonstrated that sensory denervation with the neurotoxin
capsaicin worsened the inflammation in an acute and chronic
model of experimental colitis, which suggests a protective role of
sensory nerve fibers during gut inflammation. Because we could
demonstrate that sensory neuropeptides like Calcitonin gene-related
peptide (CGRP) and substance P (SP) are released from sensory nerve
fibers during intestinal inflammation, both are strong candidates as
mediators for the protective effect of sensory neurons. In this study
we investigate the role of CGRP and SP during experimental colitis in
the rat by use of receptor antagonists against CGRP (CGRP
8-37, 1 µg/h continuous subcutaneous infusion), SP
(RP67580, a NK-1 receptor antagonist, 3 mg/kg i.p.) and an
immunoneutralizing CGRP-antibody. A mild colitis was induced by a
rectal enema containing trinitrobenzenesulfonic acid. The severity of
inflammation increased markedly after 7 days in the CGRP receptor
antagonist and CGRP-antibody group compared with the vehicle group as
determined by a macroscopic damage score (10.4 ± 1.2 and 9.6 ± 1.6 vs. 6.2 ± 2.1) by a histologic ulceration score (82 ± 8% and 73 ± 6% vs. 42 ± 23%) and by myeloperoxidase activity (19.2 ± 6.8 and 18.1 ± 5.9 vs. 8.6 ± 5.3 U/mg tissue protein),
respectively. Treatment with the specific SP receptor antagonist did
not significantly alter the severity of colitis at 7 days compared with
the control group. These data suggest that CGRP exerts mucosal
protection during chronic experimental colitis.
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