Respiratory burst plays an important role in the immune system.

These radicals are used to destroy pathogens in a process termed the respiratory burst.

Compared to other phagocytes, the respiratory burst in AM is of a greater magnitude.

Hydrogen peroxide is also generated for phagocytes in a process often referred to as a respiratory burst.

Similar to macrophages, neutrophils attack pathogens by activating a respiratory burst.

Elevated inspired oxygen concentration often becomes necessary at this stage, and they may facilitate a 'respiratory burst' in immune cells.

The lack of CR3 interferes with chemotaxis, phagocytosis, and respiratory burst.

Additionally, the respiratory burst is inhibited.

Finally, some microbes have enzymes to detoxify oxygen metabolites formed during the respiratory burst.

Respiratory burst in white blood cells induces an increased production of free radicals and oxidants such as hydrogen peroxide.

The increase in oxygen consumption, called a respiratory burst, produces reactive oxygen-containing molecules that are anti-microbial.

The macrophage produces bacteriocidal compounds (e.g., oxygen radicals) following the respiratory burst.

The pathogen is killed by the activity of digestive enzymes or following a respiratory burst that releases free radicals into the phagolysosome.

The neutrophils phagocytize H. influenzae, thereby activating an oxidative respiratory burst.

Besides being chemotactic for neutrophils, IL-8 also activates these cells to degranulate and show respiratory burst.

Another important function occurs in phagocytes (e.g. eosinophils, neutrophils, and macrophages) during the respiratory burst.

By targeting immune cells such as macrophages the bacteria will be protected against phagocytosis and destruction by respiratory burst.

In addition, there is also an enzyme-mediated 'respiratory burst', which results in the production of a set of reactive oxygen-derived compounds.

The main products of the neutrophil respiratory burst are strong oxidizing agents including hydrogen peroxide, free oxygen radicals and hypochlorite.

Under normal circumstances, the complex is latent in neutrophils and is activated to assemble in the membranes during respiratory burst.

Recognition of these organism triggers many protective patways, such as fungal uptake by phagocytosis and killing via respiratory burst.

Neutrophils phagocytise debris and bacteria and also kill bacteria by releasing free radicals in what is called a 'respiratory burst'.

Microglia in culture secrete large amounts of HO and NO in a process known as 'respiratory burst'.

The consumption of oxygen during the generation of reactive oxygen species has been termed the "respiratory burst", although unrelated to respiration or energy production.

Extracellular thymosin β would be readily oxidised to the sulfoxide in vivo at sites of inflammation, by the respiratory burst.