Oxidative stress has been implicated in the pathogenesis of asthma. We aimed at investigating the biomarkers of oxidative stress, inflammation, and tissue damage in patients with asthma in acute exacerbation and remission. We recruited 18 asthmatics admitted to hospital with acute exacerbation and 18 healthy nonsmoking controls matched for age. We evaluated plasma levels of 8-isoprostane, C-reactive protein (CRP) and total matrix metalloproteinase- (MMP-) 9 by ELISA, and MMP-9 activity by zymographic analysis. Plasma levels of 8-isoprostane and CRP were significantly elevated in acute exacerbation and decreased in remission but remained significantly higher compared to healthy controls. The activities of pro-MMP-9 were also significantly higher in acute exacerbation and decreased in remission but remained significantly higher compared to healthy controls in parallel to plasma levels of total MMP-9. These data suggest that overproduction of MMP-9 along with highly elevated levels of oxidative stress and inflammation is implicated in asthma exacerbation and that measurements of these biomarkers can be a valid index in its management. 1. Introduction Asthma is a chronic inflammatory airway disease that affects children and adults of all ages [1]. Chronic inflammation, which involves recruitment and activation of inflammatory cells, has been increasingly recognized as a mechanism leading to oxidative stress in asthma [2]. According to Wark and Gibson [3], the patterns of airway inflammation are different for different triggering factors, while the exaggerated response of asthmatic airways is still not completely well known. 8-Isoprostane is considered a marker of oxidative stress specific for lipid peroxidation, which is a stable metabolite of arachidonic acid, synthesized in vivo, and biologically active [4]. Previous studies found higher 8-isoprostane levels in the plasma, exhaled breath condensate (EBC), and induced sputum in asthmatic patients [5–7]. In the few studies carried out on patients in acute exacerbation of asthma, changes in oxidative stress have been reported, including increased plasma thiobarbituric acid reactive substances (TBARS), exhaled pentane levels, and exhaled breath 8-isoprostane in acute exacerbation versus stable asthma [8–10]. C-reactive protein (CRP), an acute-phase protein, is a highly sensitive systemic marker of inflammation, infection, and tissue damage [11]. Beside airway inflammation, several studies have indicated a positive relationship between asthma and increased CRP levels [12–17]. Recently, Fujita et al. found that
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