Biomedical Engineering Reference
In-Depth Information
Figure 1
(A) and (B): Photomicrographs showing bronchial biopsy specimens
immunostained with anti-EG-2 (eosinophil cationic protein) from a patient with
fixed airflow obstruction and a history of COPD (A) and from a patient with fixed
airflow obstruction and a history of asthma (B). The two patients had a similar
degree of fixed airflow obstruction. In (B), there is prominent eosinophilia beneath
the destroyed epithelium that is not present in (A). (C) and (D): Photomicrographs
showing bronchial biopsy specimens stained with H&E from a patient with fixed air-
flow obstruction and a history of COPD (C) and from a patient with fixed airflow
obstruction and a history of asthma (D). The two patients had a similar degree of
fixed airflow obstruction. In (D), there is a thicker reticular layer of the epithelial
basement membrane compared with (C). (From Ref. 28.)
The finding of this study suggests that asthmatic airway inflammation
does not change with the development of fixed airflow limitation and does
not become similar to the airway inflammation characteristic of COPD
(5,28). Thus, even when they develop fixed airflow limitation, patients with
a history of asthma have the same airway inflammatory changes that are pre-
sent in asthmatics with variable airflow limitation, in terms of both cellular
infiltrates and increased thickness of the reticular layer of the basement
membrane, indicating that, even when fixed airflow limitation is present,
asthma should be diagnosed and treated as asthma and not as COPD.
V. INFLAMMATORY MEDIATORS IN COPD AND ASTHMA
A. COPD
Migration and activation of inflammatory cells is regulated by cytokines and
chemokines, small proteins secreted by a variety of structural, such as
