Background/aims: Sensory nerves appear to have a protective effect against acute injury in the gastric mucosa. Their function in the intestine is unclear.
Methods: In this study an immune-complex model of colitis was used to induce inflammation in the distal colon with and without functional ablation of sensory neurons by capsaicin pretreatment.
Results: Colitis was more severe in the capsaicin-pretreated group than in the vehicle group 48 and 96 hours after induction of colitis. Neutrophil infiltration, expressed as inflammatory index, was significantly increased to 4.25 +/- 0.4 vs. 1.83 +/- 0.5 at 48 hours and to 2.66 +/- 0.6 vs. 1.65 +/- 0.3 at 96 hours in the capsaicin group and the vehicle group, respectively. The microscopic ulcer index also was significantly increased in the capsaicin-pretreated group compared with the vehicle group (63.3 +/- 10.6 vs. 3.3 +/- 2.4 at 48 hours, 20.0 +/- 8.4 vs. 1.5 +/- 1.1 at 96 hours). Immunoreactive substance P (SP) and calcitonin gene-related peptide (CGRP) contents were decreased in extracts of inflamed compared with uninflamed colon.
Conclusions: These data suggest that sensory neurons have a protective role in an acute rabbit model of experimental colitis by release of sensory neuropeptides (SP, CGRP), which may modulate vascular tone and mucosal blood flow.