Biomedical Engineering Reference
In-Depth Information
17
CHAPTER
Adhesion Molecules and Smoking
Matthew J. Garabedian
1, *
and Kristine Y. Lain
2
Department of Obstetrics and Gynecology, University of Kentucky,
800 Rose Street, Room C-358, Lexington, KY 40536-0293,
1
E-mail:
matt.garabedian@uky.edu
2
E-mail:
kylain2@email.uky.edu
Departmental Administrator
: Linda Sager, Department of Obstetrics and
Gynecology, University of Kentucky, 800 Rose Street, Room C-358, Lexington,
KY 40536-0293, E-mail:
lsage2@uky.edu
ABSTRACT
h e association between smoking and disease was identii ed prior to elucidating the
underlying molecular mechanisms. Cigarette smoke is a complex mixture of many
compounds, of which nicotine is considered the most important biologically active
agent. Exposure to cigarette smoke and nicotine creates a systemic inl ammatory
condition increasing the risk of cardiovascular disease (CVD), atherosclerosis,
asthma, and chronic obstructive pulmonary disease (COPD). Cellular adhesion
molecules play a role in these disease states. Systemic inl ammation enhances
adhesion molecule expression, which facilitates leukocyte recruitment and
migration into tissue and leads to inl ammatory injury.
In endothelial cell cultures, administration of cigarette smoke condensate and
purii ed nicotine enhances expression of adhesion molecules and inl ammatory
cytokines via second messenger signaling pathways. h ese signaling pathways
trigger altered genetic expression and the upregulation of inl ammatory cytokines.
h is correlates with the clinical understanding of atherosclerosis, asthma, and
COPD as inl ammatory conditions. In human populations, the same adhesion
molecules that are enhanced by cigarette smoke condensate and nicotine
