respiratory burst involved in inflammatory response

Definition

Target type: biologicalprocess

A phase of elevated metabolic activity, during which oxygen consumption increases following a stimulus as part of an inflammatory response; this leads to the production, by an NADH dependent system, of hydrogen peroxide (H2O2), superoxide anions and hydroxyl radicals, resulting in an increase in their intracellular or extracellular levels. [GOC:add, ISBN:0781735149]

The respiratory burst is a critical component of the inflammatory response, a complex physiological process that involves the activation of immune cells and the release of various mediators to combat infections, tissue damage, and other harmful stimuli. Here's a detailed description of the biological process:

1. **Initiation:** The respiratory burst is triggered by the activation of immune cells, primarily neutrophils and macrophages, by pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs). These patterns are recognized by pattern recognition receptors (PRRs) on the surface of immune cells.

2. **Activation of NADPH Oxidase:** Upon activation, a complex enzyme system called NADPH oxidase is assembled in the cell membrane of these immune cells. This enzyme complex consists of several subunits, including gp91phox (also known as NOX2), p22phox, p47phox, p67phox, and p40phox.

3. **Electron Transfer and Superoxide Production:** NADPH oxidase catalyzes the transfer of electrons from NADPH (nicotinamide adenine dinucleotide phosphate) to molecular oxygen (O2). This electron transfer generates superoxide radicals (O2-), a highly reactive form of oxygen. The production of superoxide is the defining characteristic of the respiratory burst.

4. **Formation of Reactive Oxygen Species (ROS):** Superoxide radicals are unstable and readily undergo further reactions, leading to the formation of other reactive oxygen species (ROS), such as hydrogen peroxide (H2O2), hydroxyl radicals (OH.), and singlet oxygen (1O2). These ROS possess potent antimicrobial and cytotoxic activities.

5. **Microbicidal and Cytotoxic Effects:** ROS generated during the respiratory burst have several effects that contribute to the inflammatory response:

* **Direct killing of microbes:** ROS can directly damage the DNA, proteins, and membranes of invading pathogens, leading to their destruction.
* **Activation of other immune cells:** ROS can signal to other immune cells, such as lymphocytes and NK cells, to participate in the inflammatory response.
* **Tissue damage and inflammation:** While ROS are essential for killing pathogens, they can also cause damage to host tissues, contributing to inflammation.

6. **Resolution of Inflammation:** The respiratory burst is a tightly regulated process. After the initial burst of ROS production, mechanisms are activated to limit the production of ROS and to repair any damage caused by them. These mechanisms include the production of antioxidant enzymes like catalase and superoxide dismutase, which neutralize ROS, and the activation of signaling pathways that promote the resolution of inflammation.

In summary, the respiratory burst is a critical process in the inflammatory response that involves the production of ROS by NADPH oxidase. These ROS play essential roles in killing pathogens, activating other immune cells, and causing tissue damage. The tightly regulated nature of the respiratory burst ensures that it effectively combats infection while minimizing damage to host tissues.'
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