endotoxintriggered

Endotoxin-triggered refers to physiological and immunological responses initiated by endotoxins, most notably lipopolysaccharide (LPS) found in the outer membrane of Gram-negative bacteria. When endotoxin enters the host, it can provoke a rapid and coordinated inflammatory reaction, ranging from fever and mild inflammation to severe systemic illness.

The primary molecular mechanism involves the recognition of LPS by a receptor complex on immune cells. Lipopolysaccharide binds to lipopolysaccharide-binding protein in circulation, is transferred to CD14, and then interacts with the TLR4–MD-2 complex. This engagement activates intracellular signaling pathways, including MyD88-dependent and TRIF-dependent routes, leading to activation of transcription factors such as NF-kB and AP-1. The result is the production of pro-inflammatory cytokines (for example TNF-α, IL-1β, IL-6), chemokines, nitric oxide, and prostaglandins. These mediators orchestrate fever, leukocyte recruitment, vascular changes, and coagulation activation, which can progress to septic shock in severe cases.

Clinically, endotoxin-triggered inflammation is central to sepsis and septic shock, as well as to sterile inflammatory states arising from endotoxin translocation. Diagnostic and therapeutic approaches focus on treating the underlying infection, supporting organ function, and exploring strategies to modulate the inflammatory response. Research continues into TLR4 antagonists, LPS-sequestration methods, and approaches to mitigate endotoxin-induced organ injury, while acknowledging mixed results in systemic sepsis management. The term is used across immunology to describe responses attributable to endotoxin exposure in both experimental and clinical contexts.