Biomedical Engineering Reference
In-Depth Information
Figure 1
Epithelium in COPD. There is enough evidence to implicate the epithe-
lium in the airways and alveolar wall as the initiator of the innate immune inflamma-
tory response in smokers. Epithelial irritation, necrosis, and apoptosis induced by
cigarette smoke would produce the necessary mediators, chemokines, and cytokines
to attract the innate inflammatory cells. The persistence of this inflammatory reac-
tion could be the key for the development of COPD.
cells (22). These findings indicate that infectious and irritant stimuli similarly
affect epithelial cells toward the production of proinflammatory mediators
and the induction of an innate immune response.
Another consequence of the injury of the epithelium by cigarette
smoke and the resultant increase in epithelial permeability (21,23) is the pro-
duction and release of tachykinins (substance P and neurokinin A). These
neuropeptides are synthesized by sensory neurons and stored in the terminal
parts of the axon collaterals found beneath and within the epithelium,
around blood vessels, submucosal glands, and within muscle layer of the air-
ways. The release of tachykinins from sensory nerves can be evoked by a
variety of stimuli including cigarette smoke (24,25) and modulate a number
of important immunological functions like T-cell proliferation (26) lympho-
cyte traffic (27), and cytokine production including IL-1, IL-3, IL-6,
IL-10, IL-12, and TNF-
a
(28,29). Thus, the bronchial epithelium, in addi-
tion to acting as a physicochemical barrier, plays a crucial role in initiating
pulmonary host defense mechanisms, both in health and in disease, by
synthesizing and releasing a variety of mediators that can cause an innate
immunity inflammatory cell differentiation, chemotaxis, and cell activation.
