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Asthma Inflammation

Oxidative stress (inflammation) is increased in the asthmatic airway, and this increased oxidative stress may play a role in the pathogenesis (how a disease develops) of asthma. Summarized studies supporting the viewpoint that oxidative stress can be a critical contributor to asthma development and can initiate various intracellular signaling pathways that lead to a break in immune tolerance and exaggerated allergic inflammation. Controlling oxidative stress at the appropriate times and with the proper methods is critical for effectively managing asthma


Asthma is a chronic inflammatory airway disease, and oxidative stress may be involved in its development. Despite an inconclusive debate about whether the enhanced oxidative stress observed in asthma subjects is caused by inflammation or is a causative factor in the development (pathogenesis) of the disease, many recent reports have supported the critical role of oxidative stress in the development of various chronic immunologic diseases. 

In bronchial asthma, oxidative stress aggravates airway inflammation by inducing diverse pro-inflammatory mediators, enhancing bronchial hyper-responsiveness, stimulating bronchospasm, and increasing mucin secretion.


Although many studies have discussed the pivotal role of enhanced oxidative stress in the development and maintenance of airway inflammation, the therapeutic effects of many antioxidant agents on allergic airway inflammation are moderate at best. These observations, however, do not necessarily imply a negligible role of oxidative stress in the pathogenesis of asthma. Rather, they reflect the need to investigate the proper antioxidants for each type of immunologic disease and the ideal situations for their use. Therefore, it is necessary to clarify the precise role of oxidative stress in the development of asthma.

It is assumed that a higher severity of asthma is also closely related to a lower ability to control oxidative stress in genetically predisposed patients.

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