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Identification of Small Molecule Modulators of Reactive Oxygen Release in TNF-a Primed Primary Human Neutrophils

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Identification of Small Molecule Modulators of Reactive Oxygen Release in TNF-a Primed Primary Human Neutrophils

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Neutrophils are components of the innate immune system with an important role in the protection against external microorganisms. Neutrophils in circulating blood are normally in a resting state, but a number of inflammatory mediators can change them into an active state by a priming procedure. Activation triggers the adhesion and penetration of neutrophils into inflamed tissue, where reactive oxygen species (ROS) are released through the activation of NADPH oxidase. Tumor necrosis factor alpha (TNF-α) is one of the earliest cytokines produced at an inflammatory site. TNF-α itself does not activate NADPH oxidase in neutrophils to a great extent, but acts as a priming agent. Upon addition of the actin filament disrupting agent cytochalasin B to TNF-α primed neutrophils, a burst of released ROS is observed, with a timing and magnitude profile resembling that observed following stimulation of proinflammatory GPCRs expressed on the neutrophil surface.

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