Contribution of alpha- and beta-defensins to lung function decline and infection in smokers: an association study

Alison M Wallace¹ , Jian-Qing He¹ , Kelly M Burkett¹ , Jian Ruan¹ , John E Connett² , Nicholas R Anthonisen³ , Peter D Paré¹ and Andrew J Sandford¹

¹James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, University of British Columbia, Vancouver, Canada

²Division of Biostatistics, School of Public Health, University of Minnesota, Minneapolis, USA

³Faculty of Medicine, University of Manitoba, Winnipeg, Canada

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Respiratory Research 2006, 7:76doi:10.1186/1465-9921-7-76


Published:	15 May 2006

Abstract

Background

Alpha-defensins, which are major constituents of neutrophil azurophilic granules, and beta-defensins, which are expressed in airway epithelial cells, could contribute to the pathogenesis of chronic obstructive pulmonary disease by amplifying cigarette smoke-induced and infection-induced inflammatory reactions leading to lung injury. In Japanese and Chinese populations, two different beta-defensin-1 polymorphisms have been associated with chronic obstructive pulmonary disease phenotypes. We conducted population-based association studies to test whether alpha-defensin and beta-defensin polymorphisms influenced smokers' susceptibility to lung function decline and susceptibility to lower respiratory infection in two groups of white participants in the Lung Health Study (275 = fast decline in lung function and 304 = no decline in lung function).

Methods

Subjects were genotyped for the alpha-defensin-1/alpha-defensin-3 copy number polymorphism and four beta-defensin-1 polymorphisms (G-20A, C-44G, G-52A and Val38Ile).

Results

There were no associations between individual polymorphisms or imputed haplotypes and rate of decline in lung function or susceptibility to infection.

Conclusion

These findings suggest that, in a white population, the defensin polymorphisms tested may not be of importance in determining who develops abnormally rapid lung function decline or is susceptible to developing lower respiratory infections.