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Respiratory Viruses Augment the Adhesion of Bacterial Pathogens to Respiratory Epithelium in a Viral Species- and Cell Type-Dependent Manner

Vasanthi Avadhanula,^1,2 Carina A. Rodriguez,^1, John P. DeVincenzo,^3,4 Yan Wang,¹ Richard J. Webby,¹ Glen C. Ulett,^1, and Elisabeth E. Adderson^1,2,3*

Department of Infectious Diseases, St. Jude Children's Research Hospital,¹ Departments of Molecular Sciences,² Pediatrics, University of Tennessee, Memphis,³ Children's Foundation Research Center, LeBonheur Children's Medical Center, Memphis, Tennessee⁴

Received 7 September 2005/ Accepted 1 December 2005

Secondary bacterial infections often complicate respiratory viral infections, but the mechanisms whereby viruses predispose to bacterial disease are not completely understood. We determined the effects of infection with respiratory syncytial virus (RSV), human parainfluenza virus 3 (HPIV-3), and influenza virus on the abilities of nontypeable Haemophilus influenzae and Streptococcus pneumoniae to adhere to respiratory epithelial cells and how these viruses alter the expression of known receptors for these bacteria. All viruses enhanced bacterial adhesion to primary and immortalized cell lines. RSV and HPIV-3 infection increased the expression of several known receptors for pathogenic bacteria by primary bronchial epithelial cells and A549 cells but not by primary small airway epithelial cells. Influenza virus infection did not alter receptor expression. Paramyxoviruses augmented bacterial adherence to primary bronchial epithelial cells and immortalized cell lines by up-regulating eukaryotic cell receptors for these pathogens, whereas this mechanism was less significant in primary small airway epithelial cells and in influenza virus infections. Respiratory viruses promote bacterial adhesion to respiratory epithelial cells, a process that may increase bacterial colonization and contribute to disease. These studies highlight the distinct responses of different cell types to viral infection and the need to consider this variation when interpreting studies of the interactions between respiratory cells and viral pathogens.

Present address: Department of Pediatrics, University of South Florida, Tampa, Fla.

Present address: School of Molecular and Microbial Sciences, University of Queensland, Brisbane, Australia.

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