Biomedical Engineering Reference
In-Depth Information
Figure 1
Macrophages may play a pivotal role in COPD as they are activated by
cigarette smoke extract and secrete many inflammatory proteins that may orches-
trate the inflammatory process in COPD. Neutrophils may be attracted by interleu-
kin (lL)-8, growth related oncogene-
a
(GRO-
a
) and leukotriene B
4
(LTB
4
),
monocytes by macrophage chemotactic protein-1 (MCP-1), and CD8
รพ
lymphocytes
by interferon-g inducible protein (IP)-10, monokine-induced by interferon-g (Mig)
and interferon-inducible T-cell
a
-chemoattractant (I-TAC). Release of elastolytic
enzymes including matrix metalloproteinases (MMP) and cathepsins cause elastoly-
sis, and release of transforming growth factor (TGF)-
b
1 and connective tissue
growth factor (CTGF). Release of TGF-
a
activates epithelial growth factor receptors
(EGFR) which stimulate mucus hypersecretion. Macrophages also generate reactive
oxygen species (ROS) and nitric oxide (NO) which together form peroxynitrite and
may contribute to steroid resistance.
long after smoking cessation. Respiratory bronchiolitis is represented by
ill-defined parenchymal micronodules detected on high resolution computer
ized tomography in some cigarette smokers. Long-term follow-up suggests
that these nodules may evolve into centrilobular emphysema and may there-
fore represent the evolution of emphysema (11).
The increased numbers of macrophages in COPD may be explained by
increased recruitment of blood monocytes into the lung, prolonged survival
within the lung, or impaired clearance of macrophages from the respiratory
tract.
A.
Increased Recruitment
The increased numbers of macrophages in smokers and COPD patients may
be explained by increased recruitment of monocytes from the circulation in
