Sepsis is a complex, life-threatening syndrome that can lead to systemic organ failure and dysfunction. Its high morbidity and mortality rates makes it a critical global health issue. The primary factors at play during sepsis are abnormal inflammation and a lack of oxygen supply to the tissues and muscles. The toll-like receptors play a crucial role in eliciting innate immune in response to infection, primarily through the interleukin-1 receptor-associated kinase (IRAK) pathways. Disturbances in the homeostasis of IRAK signaling cascades can lead to immune dysfunction. n this paper, we review the molecular mechanisms of IRAK-1, an important mediator of TLR-induced inflammation and compare the effects of its splice variants and polymorphisms in the context of inflammation and sepsis.
If you have any questions please contact the ETD Team, libetd@njit.edu.