Biomedical Engineering Reference
In-Depth Information
Table 3
Major constituents of cigarette smoke
Gaseous phase
Particulate phase
Carbon monoxide
Nicotine
Nitrogen oxides
Phenol
Ammonia
Antracyclic hydrocarbons
Hydrogen cyanide
Nitrosamines
Formaldehyde
Heavy metals (e.g., cadmium)
Acrolein
Nitroso-compounds
Benzene
Cigarette smoke is a complex mixture of over 4,000 compounds (Kalra
et al.
1994).
transcription factor NF-ĸB and expression of its products, including ICAM-1,
ELAM-1, and VCAM-1
(Fig. 2)
(Shen
et al.
1996).
Furthermore, CSC augments leukocyte migration across the endothelium
by its ef ect on PECAM-1, a platelet-derived adhesion molecule. CSC incites
phosphorylation of PECAM-1 via PKC, which alters cell-to-cell adhesion in the
endothelium. h is allows for increased leukocyte migration to the subendothelium.
Treatment with either PKC inhibitors or antibody to PECAM-1 attenuates the
af ects of CSC on leukocyte transmigration (Shen
et al.
1996).
CSC-induced Changes of Cytokine Expression
The Role of ICAM-1
h e specii c components of the CSC that are responsible for the physiological
ef ects are dii cult to determine, but nicotine alters leukocyte adhesion and
transendothelial migration. ICAM-1 and VCAM-1 are not expressed in HUVEC
cultures under physiological conditions, but exposure to nicotine induces cellular
expression of these adhesion molecules (Albaugh
et al.
2004, Ueno
et al.
2006),
mediated via expression of two pro-inl ammatory cytokines, TNF-α and IL-1β
(Zhang
et al.
2002, Albaugh
et al.
2004, Wang
et al.
2004). ICAM-1 is elevated
in the supernatant from HUVEC cultures exposed to IL-1β and to cotinine, a
bioactive nicotine metabolite. h e ICAM-1 concentration is related to cotinine
exposure in a dose-dependent fashion (Lain
et al.
2006).
Macrophage expression of sICAM-1, sVCAM-1, and sE-selectin is induced
with nicotine (Wang
et al.
2004, Ueno
et al.
2006) and associated with increased
expression of TNF-α and IL-1β. Expression of other inl ammatory cytokines (INF-γ
and IL-8) is not increased with nicotine administration, demonstrating specii city
of the TNF-α and IL-1β response of macrophages to nicotine exposure (Wang
et al.
2004). h e CSC does not directly stimulate expression of sICAM-1; rather,
