Effects of Capsaicin on Production of Cytokines and Nitric Oxide, Salmonella Infection and NF-kappa B Activation / 대한면역학회지

ABSTRACT

"Capsaicin, the pungent principle of hot peppers, is a neurotoxin that depletes primary sensory neurons of neuropeptides like tachykinin. The objectives of these experiment was to examine the effects of capsaicin on Salmonel/a typhimurium-induced production of cytokines such as TNF-a, IL-1B, IL-6, IL-10 and IL-12 and on production of nitric oxide in peritoneal macrophages. In addition, the effects of capsaicin on survival rates of S. typhimurium-infected mice and on nuclear transcription factor (NF-kB) activation were also investigated. Mice were pretreated with a single s.c. injection of 100 ug of capsaicin and were infected i.v. with S. typhimurium (5xO5/mouse) in 0.2 ml volume after capsaicin pretreatment. The serum cytokine levels were measured 30, 60, 120, 180 and 240 min after Salmonella infection, using ELISA kits. The activation of NF-B was also examined by gel shift assay in spleens, thymuses and brains of mice that had been pretreated with a single s.c. injection of 100 ug of capsaicin. It was found that Sa/mone/la infection induced the production of TNF-a, IL-1B, IL-6, IL-10 and IL-12, but capsaicin pretreatment inhibited the production of TNF-a, IL-1B, IL-10 and IL-12, but enhanced IL-6 production 120 min after Salmonella infection. Interestingly, the capsaicin pretreatment inhibited the activation of NF-kB in spleens and thymuses. There were no differences in the numbers of bacteria in livers, brains, spleens, kidneys and lungs between capsaicin- pretreated mice and the control animals in applied experimental conditions. Suprisingly, however, capsaicin pretreatment increased both the survival rates of Sa/mone//a-infected mice and production of nitric oxide by peritoneal macrophages compared with capsaicin-untreated control mice. Taken together, these results indicate that the capsaicin-sensitive primary sensory neurons may play an important modulatory role in the production of cytokine, nitric oxide and NF-B activation and the pathogenesis of salmonellosis."