The oxidative burst plays an important role in the human body's immune system. It is a crucial reaction that occurs in phagocytes to kill internalized bacteria, and it is one of the body's key defense mechanisms.
During phagocytosis in the oxidative burst, there is a rapid release of hypochlorous acid after neutrophils come into contact with different bacteria or fungi, killing them within milliseconds.
The hypochlorous acid, produced by neutrophils, destroys microorganisms by binding to critical cell membrane components and affecting cell permeability. This leads to the rupture of the cell membrane and subsequent disintegration of cells (1).
This powerful human body response is effective against a broad spectrum of the most common, harmful invading pathogens, including:
- Staphylococcus aureus
- Escherichia coli
- Enterococcus faecalis
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- Clostridium difficile
- Pseudomonas aeruginosa
- Candida albicans
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Challenges to Wound Healing
As powerful as this response is, recent studies have demonstrated an impairment of neutrophil function in diabetic mammals (2). This impairment could contribute to the high incidence of infections in diabetic foot ulcer patients. This is important because even when pathogens are present at levels below the infection threshold, slow wound healing can result.
These pathogens often aggregate within complex structural biofilm communities composed of proteins and extracellular polysaccharides, which many antibiotics have difficulty penetrating. Left unresolved, this biofilm can be a contributing cause to delayed wound healing and the consequences of inflammatory responses.
References
1. McKenna et al., (1988). Biochem J., 254:685-692.
2. Alba-Loureiro et al., (2006). Journal of Endocrinology, 188:295-303.