ABSTRACT
The anti-inflammatory cytokines interleukin-10 (IL-10) and interleukin-13 (IL-13) were shown to reduce hyperalgesia in some models such as rats exposed to UV rays. In addition, IL-10 was also shown to reduce hyperalgesia in high dose of Leishmania major-induced inflammation in BALB/c mice accompanied by a significant decrease in the levels of interleukin-1ß (IL-1ß) in the paws of infected mice, while no effect on the levels of IL-6 was observed. In this study, we injected BALB/c mice with a high dose of L. major and treated them with IL-13 (15 ng/animal) for twelve days (excluding the weekends) and hyperalgesia was assessed using thermal pain tests. Furthermore, the levels of IL-1ß and IL-6 were also assessed at different post-infection days. Our results show that IL-6 and more importantly IL-1ß don't play a direct role in the L. major-induced hyperalgesia and that IL-13 induces this hyperalgesia through the down-regulation of IL-1ß and another proinflammatory cytokine (most probably TNF-α). Furthermore, our data show that IL-13 leads to the upregulation of the level IL-6 which initially seems to have no direct role in the induced hyperalgesia. Therefore, we suggest that the L. major-induced hyperalgesia is mainly mediated by the cytokine cascade leading to the production of sympathetic amines.
