including inflammatory mediator production, changes in blood coagulation system and microvascular permeability was denoted as systemic inflammatory response syndrome (SIRS) [32] . On the other hand, we proposed that the prominent production of IL-10 from the early stages of the experimental HPAI infection was the compensatory response to overproduction of proinflammatory cytokines such as TNF-α, IL-6 and IL-12. However, the role of IL-10, which principle function seems to be containment and eventual termination of inflammation [33] , in HPAI pathogenesis is unclear. Also there is an uncertain discrepancy between undetectable expression of IL-18 and high levels of other Th1-cytokines (IFN-γ and IL-12).