Abstract
Sepsis is a systemic inflammatory response syndrome in response to severe infection. An overwhelming systemic response brought about by the release of various inflammatory mediators can lead to shock, multiple organ damage and death. Cytokines play an important role in the pathogenesis of sepsis and are regulated by a complex network of pro- and anti-inflammatory mediators. Various chemokines sequester neutrophils into the target organ, further augmenting inflammation. Chemokine receptor antagonism represents a major therapeutic approach against sepsis. Adhesion molecules mediate the migration of leukocytes towards the site of inflammation and their activation. Gaseous mediators such as nitric oxide and hydrogen sulfide are also involved in the pathogenesis of inflammation. Our review summarizes the current understanding of the roles of various inflammatory mediators in sepsis.