Capsaicin is the active ingredient in chili pepper and has an inhibitory effect on Helicobacter pylori growth and $NF-{kappa}B$ activation. The present study examined the effect of capsaicin on interleukin (IL)-8 production by H. pylori ATCC 43504-infected MKN-45 cells, a gastric epithelial cell line. The viability of the MKN-45 cells treated with capsaicin at 0, 50, 100, 250, and $500;{mu}M$ was 99, 98, 99, 99, and 85%, respectively. A capsaicin concentration as low as $50;{mu}M$ significantly inhibited the IL-8 production induced by H. pylori ATCC 43504 infection (43.2% of control) during 24 h of incubation. However, low concentrations of capsaicin $(50;and;100{mu}M)$ did not significantly inhibit the IL-8 production by $TNF-{alpha}-$ or PMA-treated MKN-45 cells. Therefore, the overall inhibitory effect of capsaicin on H. pylori ATCC 43504 was the sum of H. pylori ATCC 43504 growth inhibition, host cell survival, and $NF-{kappa}B$ signal cascade inhibition.