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1 Division of Gastroenterology,
We have previously
reported that pretreatment of rats with capsaicin (an agent that
ablates sensory neurons) or CP-96345 (a substance P receptor
antagonist) dramatically inhibits fluid secretion and intestinal
inflammation in ileal loops exposed to Clostridium difficile toxin A. The aim of this study was to
determine whether calcitonin gene-related peptide (CGRP), a
neuropeptide also found in sensory afferent neurons, participates in
the enterotoxic effects of toxin A. Administration of toxin A was also
found to increase CGRP content in dorsal root ganglia and ileal mucosa
60 min after toxin exposure. Furthermore, immunohistochemical studies
demonstrated increased neuronal staining for CGRP 2 h after toxin A
treatment. Pretreatment of rats with CGRP-(8
37), a specific CGRP
antagonist, before instillation of toxin A into ileal loops
significantly inhibited toxin-mediated fluid secretion (by 48%),
mannitol permeability (by 83%), and histological damage. We conclude
that CGRP, like substance P, contributes to the secretory and
inflammatory effects of toxin A via increased production of this
peptide from intestinal nerves, including primary sensory afferent
neurons.
intestine; sensory nerves; neurotransmitters; calcitonin gene-related peptide
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