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

Biomedical and clinical sciences 1109 Insect Science Medical bacteriology Syncytial-virus Blotting, Western Gene Expression Tract Infections Expression Platelet Membrane Glycoproteins Respiratory Mucosa Polymerase Chain Reaction Bacterial Adhesion Receptors, G-Protein-Coupled 03 medical and health sciences veterinary and food sciences Antigens, CD Virology Cell Line, Tumor Humans RNA, Messenger Children Cells, Cultured Agricultural 2403 Immunology 0303 health sciences Streptococcus-pneumoniae 2404 Microbiology Mucins Epithelial Cells Platelet-activating-factor Intercellular Adhesion Molecule-1 Haemophilus influenzae Parainfluenza Virus 3, Human Respiratory Syncytial Viruses 3. Good health Biological sciences Influenza A virus Obstructive Pulmonary-disease Lethal Synergism 2406 Virology Factor Receptor Cell Adhesion Molecules Nontypable Haemophilus-influenzae
DOI: 10.1128/jvi.80.4.1629-1636.2006 Publication Date: 2006-01-26T18:02:43Z
ABSTRACT
ABSTRACT 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 S treptococcus 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.
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