Action of sensory neurons in an experimental at colitis model of injury and repair.

The influence of sensory nerves on inflammation and healing was studied in a rat colitis model at different stages of inflammation. Studies were performed in animals with and without ablation of sensory nerves, which was achieved by pretreatment with the neurotoxin capsaicin. Colitis was induced by a rectal enema containing trinitrobenzenesulfonic acid (50 mg/kg) in 50% ethanol. Severity of inflammation was markedly increased 3 and 7 days after induction of colitis in the capsaicin-pretreated group compared with the vehicle group as determined by a macroscopic damage score (at 3 days, 12.0 +/- 0.7 vs. 7.5 +/- 1.5; at 7 days, 12.2 +/- 0.8 vs. 6.5 +/- 0.8; P < 0.05), by histology (ulceration score at 3 days, 82 +/- 12 vs. 40 +/- 11%; at 7 days, 92 +/- 5 vs. 46 +/- 13%; P < 0.05), and by myeloperoxidase activity (at 3 days, 133 +/- 30 vs. 42 +/- 14 U/mg protein; at 7 days, 76 +/- 11 vs. 39 +/- 11 U/mg protein; P < 0.05). There was no significant difference in the severity of colitis 14 and 21 days after induction of colitis between the capsaicin-pretreated group and the vehicle group. These data suggest that, in this model, sensory nerves have an important protective function in the acute and subacute phases of inflammation but do not seem to play a significant role in the later stages of chronic inflammation.