Published ahead of print on April 24, 2003, doi:10.1165/rcmb.2002-0143OC Am. J. Respir. Cell Mol. Biol., Volume 29, Number 4, October 2003, 472-482 A more recent version of this article appeared on October 1, 2003
Submitted on August 2, 2002 Smoke and C5a induce airway epithelial ICAM-1 and cell adhesionAnthony A Floreani1*,1 Pulmonary and Critical Care Medicine, University of Nebraska Medical Center, Omaha, NE, USA, 2 Allied Health Sciences, University of Nebraska Medical Center, Omaha, NE, USA, 3 Preventive and Societal Medicine, University of Nebraska Medical Center, Omaha, NE, USA, 4 Molecular Chemistry, Brown University, Providence, RI, USA * To whom correspondence should be addressed. E-mail: aflorean{at}unmc.edu.
The human bronchial epithelial cell is one of the first cell types to be exposed to the irritants and toxins present in inhaled cigarette smoke. The ability of the bronchial epithelium to modulate inflammatory and immune events in response to cigarette smoke is important in the pathogenesis of smoke-induced airway injury. We have shown that cigarette smoke extract and the complement anaphylatoxin C5a both independently induce increased expression of ICAM-1 on airway epithelial monolayers compared to unstimulated cells in vitro. This enhanced ICAM-1 expression is associated with a greater capacity of the airway epithelial cells to bind mononuclear cells, a process that appears to require the pro-inflammatory cytokine TNF-
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and PKC intracellular signaling. Exposure of epithelial monolayers to the combination of cigarette smoke followed by C5a results in an additive response for ICAM-1 expression and mononuclear cell adhesion compared to smoke or C5a challenge alone. Inhibiting C5a receptor expression can attenuate these responses. These findings suggest that smoke exposure in some way enhances the functional responsiveness of the C5a receptor expressed on these airway epithelial cells for subsequent C5a-mediated increases in ICAM-1 expression and mononuclear cell adhesion. Our results may help explain the initiation and propagation of inflammatory events in vivo induced by chronic airway exposure to cigarette smoke.
