Respiratory viruses augment the adhesion of bacterial pathogens to respiratory epithelium in a viral species- and cell type-dependent manner.
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.
Avadhanula
Vasanthi
V
Department of Infectious Diseases, St. Jude Children's Research Hospital, Mailstop 320, 332 N. Lauderdale St., Memphis, TN 38105, USA.
Rodriguez
Carina A
CA
Devincenzo
John P
JP
Wang
Yan
Y
Webby
Richard J
RJ
Ulett
Glen C
GC
Adderson
Elisabeth E
EE
D015703:Antigens, CD / Q000032:analysis; D001422:Bacterial Adhesion / Q000502:physiology*; D015153:Blotting, Western; D015815:Cell Adhesion Molecules / Q000032:analysis; D045744:Cell Line, Tumor; D002478:Cells, Cultured; D004847:Epithelial Cells / Q000382:microbiology / Q000821:virology; D015870:Gene Expression; D006193:Haemophilus influenzae / Q000502:physiology; D006801:Humans; D009980:Influenza A virus / Q000502:physiology*; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D009077:Mucins / Q000235:genetics; D010224:Parainfluenza Virus 3, Human / Q000502:physiology*; D010980:Platelet Membrane Glycoproteins / Q000032:analysis; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000032:analysis; D043562:Receptors, G-Protein-Coupled / Q000032:analysis; D020545:Respiratory Mucosa / Q000382:microbiology* / Q000821:virology*; D012136:Respiratory Syncytial Viruses / Q000502:physiology*; D013296:Streptococcus pneumoniae / Q000502:physiology
D015703:Antigens, CD; C069847:CD66 antigens; D015815:Cell Adhesion Molecules; D009077:Mucins; D010980:Platelet Membrane Glycoproteins; D012333:RNA, Messenger; D043562:Receptors, G-Protein-Coupled; C039351:platelet activating factor receptor; D018799:Intercellular Adhesion Molecule-1