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LPS-Induced Cytokines in Mice

Bacteria, viruses and other microorganisms invade the host organism, causing various immune cells in the host to produce cytokines and chemokines, forming an immune defense mechanism. In order to explore the immune pathways and the treatment of immune diseases, various infection models have been established, such as the bacterial injection infection model, endotoxin model, traumatic infection model and so on. Among them, the endotoxin model allows easy exclusion of other interfering factors, is conducive to studying the mechanisms of individual components of bacteria during infection, and provides a better experimental model for the treatment and prevention of septic shock.

Lipopolysaccharide (LPS) belongs to the pathogen-associated molecular pattern (PAMP). It can activate the mononuclear phagocytic system (MPS), cause the release of THF-a, IL-12, IFN-y and other inflammatory mediators, lead to systemic excessive inflammatory response, and ultimately lead to necrosis in the brain, heart, lung, kidney, liver and other organs. The immunopathological feature of the LPS model is overactivation of the innate immune response, accompanied by a large number of inflammatory cytokines, such as IL-6, IL-1 and, most crucially, TNF.

LPS-Induced Cytokine Production in Mouse Plasma

Aim: To examine the effect of prednisone on LPS-induced TNF-α production in mice.

Animal: BALB/c mice

Reagent: LPS

Mouse TNF-α kit: R&D System

Effect of Prednisone on LPS-Induced TNF-α Production

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