M. Reinshagen et al., ACTION OF SENSORY NEURONS IN AN EXPERIMENTAL RAT COLITIS MODEL OF INJURY AND REPAIR, American journal of physiology: Gastrointestinal and liver physiology, 33(1), 1996, pp. 79-86
The influence of sensory nerves on inflammation and healing was studie
d 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. Col
itis 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-pre
treated group compared with the vehicle group as determined by a macro
scopic damage score (at 3 days, 12.0 +/- 0.7 vs. 7.5 +/- 1.5; at 7 day
s, 12.2 +/- 0.8 vs. 6.5 +/- 0.8; P < 0.05), by histology (ulceration s
core 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/m
g protein; P < 0.05). There was no significant difference in the sever
ity of colitis 14 and 21 days after induction of colitis between the c
apsaicin-pretreated group and the vehicle group. These data suggest th
at, in this model, sensory nerves have an important protective functio
n in the acute and subacute phases of inflammation but do not seem to
play a significant role in the later stages of chronic inflammation.