Biomedical Engineering Reference
In-Depth Information
Figure 2
Mechanisms of ROS-mediated lung inflammation in COPD and genera-
tion of potential biomarkers. Inflammatory response is mediated by oxidants either
inhaled and
=
or released by the activated neutrophils, alveolar macrophages, eosino-
phils, and epithelial cells leading to production of ROS and membrane lipid perox-
idation. Activation of transcription of the pro-inflammatory cytokine and chemokine
genes, upregulation of adhesion molecules and increased release of pro-inflammatory
mediators which are involved in the inflammatory responses in patients with COPD.
expiratory volume in one second (FEV
1
) an develop the disease (6). An
increased oxidant burden in smokers derives from the fact that cigarette
smoke contains more than 10
15
oxidant
=
free radical molecules per puff.
Many of these molecules are relatively long-lived such as tar-semiquinone
which can generate
OH and hydrogen peroxide (H
2
O
2
) by the Fenton reac-
tion (7,8). Other factors, such as air pollutants, infections, and occupational
dusts that may exacerbate COPD, also have the potential to produce oxida-
tive stress (9) (Fig. 2).
III. CELL-DERIVED ROS
A common feature of COPD is the development of an inflammatory
response, characterized by activation of epithelial cells, and resident macro-
phages, and the recruitment and activation of neutrophils, eosinophils,
