Abstract
Despite some advances that have been made in the clinical management of sepsis, its morbidity and mortality rates remain high. The pathogenesis of systemic inflammation and organ damage leading to septic mortality is not fully understood. Interleukin-33 (IL-33), a new member of the IL-1 superfamily, can be a traditional cytokine and a nuclear factor regulating gene transcription. Due to its biological characteristics, IL-33 can act as a double-edged sword in sepsis: It not only contributes to clear bacteria and improves survival but also causes inflammation, immunosuppression, and organ damage via modulating immune response. In this review, we will summarize updated information on the dual functions of IL-33 in the host immune response to sepsis.