Abstract
Inflammatory suppressive effects of nicotine have been observed in inflammatory diseases. We aimed to investigate morphological damage and the changes in TNF-α, IL-1β, and IL-10 expression in the healthy stomach after long-term oral nicotine administration. Nicotine was added to the drinking water of Sprague Dawley rats for 6 weeks. Histological signs of damage, inflammatory cytokines, and nicotinic acetylcholine receptor (nAChR) levels were evaluated in the gastric tissues. There were no histological signs of inflammation in both groups. TNF-α and IL-1β were decreased in the nicotine-treated group. A positive correlation was found between TNF-α levels and infiltrated inflammatory cell count. nAChR levels were increased in the nicotine group. Long term nicotine administration upregulates and activates nAChR. The reduced TNF-α or with high activity nAChR affects the modulation of neutrophil functions and its entry into tissue. Nicotine may deteriorate host defence in non-inflammatory situations.
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