Biomedical Engineering Reference
In-Depth Information
the slow-reacting substances of anaphylaxis that increase vascular perme-
ability and mucus secretion and are potent stimulators of smooth-muscle
contraction. Lastly, activated eosinophils produce a wide range of inflam-
matory cytokines that have the potential to modulate multiple aspects of
the immune response (92).
It has also recently become clear that eosinophils are not only key
effector cells in mediating asthmatic inflammation, but also have a role in
presenting allergen to stimulate CD4
þ
T-helper (Th) cells (93). Epithelial
damage and loss caused by eosinophil-derived mediators, particularly their
highly basic granule proteins—MBP, eosinophil peroxidase and ECP—is
thought to be a major event in asthma pathogenesis (94). Thus, it can be
appreciated that eosinophils have the ability to make a major contribution
to the inflammatory processes underlying asthmatic and allergic disease.
Furthermore, it is also becoming increasingly apparent that eosinophil-
epithelial cell interactions are an important facet of asthmatic disease in
relation to both the initiation and resolution of inflammation (95).
Further evidence of an inflammatory response in asthma is the pre-
sence of cytokines that mediate inflammation and chemotactic chemokines
in BALF or pulmonary secretions. Since these cytokines and chemokines
are elaborated by resident and inflammatory cells in airways and have many
effects on these cells, a variety of autocrine, paracrine, and endocrine net-
works could participate in asthma (19). Some cytokines initiate inflamma-
tory responses by activating transcription factors, which are proteins that
bind to the promoter region of genes. Transcription factors involved in
asthmatic inflammation include NF-
k
B, activator protein-1, nuclear factor
of activated T cells, cyclic AMP response-element binding protein, and
various members of the family of signal transduction-activated transcrip-
tion (STAT) factors (19). These transcription factors act on genes that
encode inflammatory cytokines, chemokines, adhesion molecules, and other
proteins that induce and perpetuate inflammation. Corticosteroids modulate
immuno inflammatory responses in asthma by inhibiting these transcription
factors (19).
The ability of cytokines to induce the expression of adhesion molecules
such as intercellular adhesion molecule 1, vascular-cell adhesion molecule 1,
and endothelial-leukocyte adhesion molecule provides a mechanism for the
adhesion of inflammatory cells to the endothelium and the migration of
these cells from the circulation into the lamina propria, the epithelium,
and in many cases, the airway lumen itself.
VI. CONCLUSIONS
Inflammation is important both in COPD and asthma, and the inflammatory
response in COPD is markedly different from that in asthma (Table 3).
