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Infect. Immun. doi:10.1128/IAI.00499-08
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Serial isolates of persistent Haemophilus influenzae in patients with chronic obstructive pulmonary disease express diminishing quantities of the HMW1 and HMW2 adhesins

Departments of Pediatrics and Molecular Genetics and Microbiology, Duke University Medical Center, DUMC 3352, Durham, NC 27710; Department of Pediatrics, Washington University School of Medicine, 660 S. Euclid Ave., St. Louis, MO 63110; Department of Internal Medicine, University of Iowa Carver College of Medcine, Iowa City, IA; University at Buffalo, State University of New York and the Veterans Affairs Western New York Healthcare System, Buffalo, NY

^* To whom correspondence should be addressed. Email: j.stgeme{at}duke.edu.

	Abstract

In patients with chronic obstructive pulmonary disease (COPD), the lower respiratory tract is commonly colonized by bacterial pathogens, including nontypeable Haemophilus influenzae. The H. influenzae HMW1 and HMW2 adhesins are homologous proteins that promote bacterial adherence to respiratory epithelium and are the predominant targets of the host immune response. These adhesins undergo graded phase variation, controlled by the number of 7-base pair repeats upstream of the HMW1 and HMW2 structural genes (hmw1A and hmw2A, respectively). In this study, we examined the levels of HMW1 and HMW2 expressed by H. influenzae isolates collected serially from patients with COPD. We found that expression of HMW1 and HMW2 in a given strain decreased over time in a majority of patients, reflecting a progressive increase in the number of 7-base pair repeats and associated with high serum titers of HMW1/HMW2-specific antibodies. We speculate that the presence of high antibody titers against the HMW1 and HMW2 adhesins and other immune factors in the lower respiratory tract of patients with COPD may result in gradual selection for bacteria with reduced levels of HMW1 and HMW2.