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Decreased Expression of Intelectin 1 in the Human Airway Epithelium of Smokers Compared to Nonsmokers¹

Brendan J. Carolan^*,, Ben-Gary Harvey, Bishnu P. De^*, Holly Vanni and Ronald G. Crystal^2,*,

^* Department of Genetic Medicine and Division of Pulmonary and Critical Care Medicine, Weill Medical College of Cornell University, New York, NY 10021

Lectins are innate immune defense proteins that recognize bacterial cell wall components. Based on the knowledge that cigarette smoking is associated with an increased risk of infections, we hypothesized that cigarette smoking may modulate the expression of lectin genes in airway epithelium. Affymetrix microarrays were used to survey the expression of lectin genes in large airway epithelium from nine nonsmokers and 20 healthy smokers and in small airway epithelium from 13 nonsmokers and 20 healthy smokers. There were no changes (>2-fold change; p < 0.05) in lectin gene expression among healthy smokers compared with nonsmokers except for down-regulation of intelectin 1, a lectin that binds to galactofuranosyl residues in bacterial cell walls (large airway epithelium, p < 0.01; small airway epithelium, p < 0.01). This was confirmed by TaqMan RT-PCR in both large (p < 0.05) and small airway epithelium (p < 0.02). Immunohistochemistry assessment of airway biopsies demonstrated that intelectin 1 was expressed in secretory cells, while Western analysis confirmed the decreased expression of intelectin 1 in airway epithelium of healthy smokers compared with healthy nonsmokers (p < 0.02). Finally, compared with healthy nonsmokers, intelectin 1 expression was also decreased in small airway epithelium of smokers with lone emphysema and normal spirometry (n = 13, p < 0.01) and smokers with established chronic obstructive pulmonary disease (n = 14, p < 0.01). In the context that intelectin 1 plays a role in defense against bacteria, its down-regulation in response to cigarette smoking is another example of the immunomodulatory effects of smoking on the immune system and may contribute to the increase in susceptibility to infections observed in smokers.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ These studies were supported, in part, by National Institutes of Heath Grants R01 HL074326, P50 HL084936, and M01RR00047 and by the Will Rogers Memorial Fund, Los Angeles, CA.

² Address correspondence and reprint requests to Dr. Ronald G. Crystal, Department of Genetic Medicine, Weill Medical College of Cornell University, 1300 York Avenue, Box 96, New York, New York 10021. E-mail address: geneticmedicine{at}med.cornell.edu

³ Abbreviations used in this paper: COPD, chronic obstructive pulmonary disease; GOLD, Global Initiative for Chronic Obstructive Lung Disease.

⁴ The online version of this article contains supplemental material.