Biomedical Engineering Reference
In-Depth Information
9
T-Lymphocytes
Manuel G. Cosio
McGill University and Royal Victoria Hospital, Montreal, Quebec, Canada
I.
INTRODUCTION
The global initiative workshop summary for chronic obstructive lung disease
(GOLD) defines COPD as a disease state characterized by airflow limitation
that is not fully reversible. The airflow limitation is usually both progressive
and associated with an abnormal inflammatory response of the lungs to nox-
ious particles or gases (1). This definition is of interest because, for the first
time, the importance of the inflammatory component in COPD is high-
lighted inviting a broader look at the possible pathogenic events in COPD,
beyond the classical, and limiting, proteinase-antiproteinase paradigm.
The implication of an inflammatory response to the pathogenesis of
emphysema, at least centrilobular emphysema, is not new. McLean in
1956 (2) and Leopold and Gough in 1957 (3) linked an inflammatory
response in the lung parenchyma to the mechanism of lung destruction,
but because their studies were based on autopsy specimens, frequently con-
taminated by terminal bronchopneumonia, this suggestion was interpreted
conservatively. Later, in 1961, Anderson and Foraker (4) observed that
the earliest pathological abnormality in centrilobular emphysema was
hypercellularity within the alveolar wall and proposed a pathogenic role
for the increased inflammatory cells in the pathogenesis of lung destruction.
The study of the inflammatory reaction in the lungs of smokers
became possible shortly after with the advent of the relatively noninvasive
fiber optic bronchoscope and BAL. Hunninghake and Crystal (5) and
Martin et al. (6), utilizing the fiberoptic bronchoscope, showed that young
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