Abstract
BackgroundViral upper respiratory tract infections are associated with increased colonization by Streptococcus pneumoniae but the mechanisms underlying this relationship are unclear. The objective of this study is to describe a comprehensive picture of the cellular interaction between the adhering bacteria and host cells in the presence or absence of a viral co-infection.ResultsGene expression profiles of Detroit-562 pharyngeal cells, which were either mock-infected or infected with human respiratory syncytial virus (RSV) or human parainfluenza virus 3 (HPIV3), were analyzed using human microarrays. Transcription response of S. pneumoniae strain TIGR4 (serotype 4) in the presence of either mock- or viral-infected cells was analyzed by pneumococcal microarray. Significantly regulated genes were identified by both significance analysis of microarray (SAM) and a ≥ 2-fold change ratio cut-off. The adherence of S. pneumoniae to human pharyngeal cells was significantly augmented in the presence of RSV or HPIV3 infection. Global gene expression profiling of the host cells during infection with RSV or HPIV3 revealed increased transcription of carcinoembryonic antigen-related cell adhesion molecules (CEACAM1), CD47, fibronectin, interferon-stimulated genes and many other host cell adhesion molecules. Pneumococci increased transcription of several genes involved in adhesive functions (psaA, pilus islet), choline uptake and incorporation (lic operon), as well as transport and binding.ConclusionsWe have identified a core transcriptome that represents the basic machinery required for adherence of pneumococci to D562 cells infected or not infected with a virus. These bacterial genes and cell adhesion molecules can potentially be used to control pneumococcal adherence occurring secondary to a viral infection.
Highlights
Viral upper respiratory tract infections are associated with increased colonization by Streptococcus pneumoniae but the mechanisms underlying this relationship are unclear
Studies of polymicrobial interactions have revealed that cellular receptors such as CD14, CD15, CD18, carcinoembryonic antigen-related cell adhesion molecule (CEACAM), macrophage receptor (MARCO), platelet-activating factor (PAFR), fibronectin (FN) and fimbriae-associated receptors are likely to be involved in increased bacterial adherence after viral infection [9,11,14,18,19,20,21]
Effect of respiratory syncytial virus (RSV) and human parainfluenza virus 3 (HPIV3) infection on the adherence of S. pneumoniae to human pharyngeal cells D562 cells were permissive to infection with RSV and HPIV3, with discrete cytopathic effect (CPE) after 72 h but without much detachment of the monolayers allowing for pneumococcal adherence
Summary
Viral upper respiratory tract infections are associated with increased colonization by Streptococcus pneumoniae but the mechanisms underlying this relationship are unclear. Several studies have demonstrated suppression of the host’s immune response as a potential mechanism for bacterial superinfection, the degree of bacterial infection induced by prior viral infection is indistinguishable from that shown using experimental models without a complete immune system e.g. in vitro adhesion assays. This suggests separate or additional mechanisms of action that are independent of immune mechanisms. The full range of adhesion molecules that can be up-regulated during a respiratory viral infection and facilitate bacterial attachment and entry is still unknown
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