Abstract:
Recent researches demonstrated the presence of a sustained hyperalgesic state in all
BALB/c mice (known to be susceptible to Leishmania major) inoculated with a high dose
of Leishmania major (2.5 x 106 promastigotes per hind paw) as shown by the evident
decrease in their pain thresholds. However, no neural involvement has been reported to
date about role of IL-Ira and IL-13 on Leishmania major-induced inflammation as
model. Thus, we aim in this project to prove the hypoalgesic effect of IL-lra and IL-13
by reversing hyperalgesia in BALB/c mice induced by Leishmania major as a new model
since other previous studies showed the anti-inflammatory effect of IL-lra and IL-13
using different models (Saade et ai., 2000; Safieh-Garabedian et ai., 1997a; Cunha et ai.,
2000).
This hyperalgesia should be accompanied with a significant increase in the levels of proinflammatory
cytokines IL-l/3 and IL-6 as is the case in the mice injected with a high
dose of the parasite (Hirano, 1998; Kanaan et ai., 2000). Both IL-lra and IL-13 had the
same effect on IL-l/3 and reduced its levels which indicate its involvement in
hyperalgesia directly. This confirms that both IL-lra and IL-13 are hypoalgesic.
Alternatively the two former cytokines had different effect on IL-6 which our results
showed its indirect effect on hyperalgesia mechanism. IL-lra decreased IL-6 levels while
IL-13 increased it. It seems that IL-6 playas a mediator IL-6 to induce hyperalgesia by
stimulation of other pro inflammatory and anti-inflammatory cytokines (Dinarello, 1994,
1997).
