TREM1 and Sepsis: Engagement of TREM-1 has been shown to induce the production of proinflammatory chemokines such as interleukin (IL-8) and cytokines such as tumour necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) [5, 6], which have been implicated in ventricular dysfunction (depress ventricular contractility) associated with a variety of pathological conditions [7], including reperfusion injury and sepsis.