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- W4386636619 abstract "Abstract Background Lipopolysaccharide, a highly potent endotoxin responsible for severe sepsis, is the major constituent of the outer membrane of gram-negative bacteria. Endothelial cells participate in both innate and adaptive immune responses as the first cell types to detect lipopolysaccharide or other foreign debris in the bloodstream. Endothelial cells are able to recognize the presence of LPS and recruit specific adaptor proteins to the membrane domains of TLR4, thereby initiating an intracellular signaling cascade. However, lipopolysaccharide binding to endothelial cells induces endothelial activation and even damage, manifested by the expression of proinflammatory cytokines and adhesion molecules that lead to sepsis. Main findings LPS is involved in both local and systemic inflammation, activating both innate and adaptive immunity. Translocation of lipopolysaccharide into the circulation causes endotoxemia. Endothelial dysfunction, including exaggerated inflammation, coagulopathy and vascular leakage, may play a central role in the dysregulated host response and pathogenesis of sepsis. By discussing the many strategies used to treat sepsis, this review attempts to provide an overview of how lipopolysaccharide induces the ever more complex syndrome of sepsis and the potential for the development of novel sepsis therapeutics. Conclusions To reduce patient morbidity and mortality, preservation of endothelial function would be central to the management of sepsis. Graphical Abstract" @default.
- W4386636619 created "2023-09-13" @default.
- W4386636619 creator A5015102287 @default.
- W4386636619 creator A5032444982 @default.
- W4386636619 creator A5066388407 @default.
- W4386636619 creator A5083654638 @default.
- W4386636619 date "2023-09-12" @default.
- W4386636619 modified "2023-10-09" @default.
- W4386636619 title "Bacterial lipopolysaccharide-induced endothelial activation and dysfunction: a new predictive and therapeutic paradigm for sepsis" @default.
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