Inflammatory stimuli of any kind, including infection, trauma, or ischemia, generate marginalization, extravasation and activation of the granulocytes and monocytes, resulting in release of pro-inflammatory cytokines such as interleukin–1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor (TNF-α), which stimulate the production of acute phase reactants. Here, IL1B is linked to infection.