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
AUTHORS (7)
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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