ABSTRACT

Infective and non-infective stimuli such as trauma and pancreatitis lead to SIRS and the release of pro-inflammatory cytokines such as tumour necrosis factor (TNF), interleukin 1 (IL1) and interleukin 6 (IL-6), with the aim of destroying damaged tissues and promoting repair. Anti-inflammatory mediators such as interleukin 10 (IL-10) are subsequently released to regulate the inflammatory response and restore homeostasis. Although inflammation is an essential host response, excessive levels of pro-inflammatory cytokines lead to systemic endothelial damage, while high levels of anti-inflammatory mediators can result in immune suppression. Inflammatory cytokines cause increased synthesis of nitric oxide (NO), which is a potent vasodilator leading to decreased systemic vascular resistance, characteristic of shock.