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Pandemic H1N1 Influenza A Directly Induces a Robust and Acute Inflammatory Gene Signature in Primary Human Bronchial Epithelial Cells Downstream of Membrane Fusion

ABSTRACT: Pandemic H1N1 influenza A (H1N1pdm) elicits stronger pulmonary inflammation than previously circulating seasonal H1N1 influenza A (sH1N1), yet mechanisms of inflammatory activation in respiratory epithelial cells during H1N1pdm infection are unclear. We investigated host responses to H1N1pdm / sH1N1 infection and virus entry mechanisms in primary human bronchial epithelial cells in vitro. H1N1pdm infection rapidly initiated a robust inflammatory gene signature (3 h post-infection) not elicited by sH1N1 infection. Protein secretion inhibition had no effect on gene induction. Infection with membrane fusion deficient H1N1pdm failed to induce robust inflammatory gene expression which was rescued with restoration of fusion ability, suggesting H1N1pdm directly triggered the inflammatory signature downstream of membrane fusion. Investigation of intra-virion components revealed H1N1pdm viral RNA (vRNA) triggered a stronger inflammatory phenotype than sH1N1 vRNA. Thus, our study is first to report H1N1pdm induces greater inflammatory gene expression than sH1N1 in vitro due to direct virus-epithelial cell interaction.

ORGANISM(S): Homo sapiens

PROVIDER: GSE48575 | GEO | 2016/07/04

SECONDARY ACCESSION(S): PRJNA210737

REPOSITORIES: GEO

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Project description:Background: Swine influenza is a highly contagious viral infection in pigs affecting the respiratory tract that can have significant economic impacts. Streptococcus suis serotype 2 is one of the most important post-weaning bacterial pathogens in swine causing different infections, including pneumonia. Both pathogens are important contributors to the porcine respiratory disease complex. Outbreaks of swine influenza virus with a significant level of co-infections due to S. suis have lately been reported. In order to analyze a global response to the dual infection, we carried out a comprehensive gene expression profiling using a microarray approach to study the swine tracheal epithelial (NPTr) cell response to a co-infection with H1N1 swine influenza virus (swH1N1) and S. suis serotype 2. Results: Gene clustering showed that the swH1N1 and swH1N1/S. suis infections modified the expression of genes in a similar manner. Additionally, infection of NPTr cells by S. suis alone did not result in many differentially expressed genes compared to mock-infected cells. However, some important genes coding for inflammatory mediators, such as chemokines, interleukins, cell adhesion molecules and eicosanoids, were significantly upregulated in the presence of both pathogens comparing to infection with each pathogen taken individually. This synergy may also be the consequence of an increased adhesion/invasion of epithelial cells previously infected by swH1N1, as recently reported. Conclusion: In a co-infection situation, influenza virus would replicate in the respiratory epithelium inducing an inflammatory infiltrate comprised of mononuclear cells and neutrophils. Despite that these cells are unable to phagocyte and kill S. suis, they are highly activated by this pathogen. S. suis is not considered a primary pulmonary pathogen, but an exacerbated production of pro-inflammatory mediators during a co-infection with influenza virus may be of critical importance in the pathogenesis and outcome of this respiratory disease complex. Total RNA obtained from NPTr cells infected with S. suis, H1N1, or S. suis & H1N1. Four replicates in both groups.

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Pandemic H1N1 Influenza A Directly Induces a Robust and Acute Inflammatory Gene Signature in Primary Human Bronchial Epithelial Cells Downstream of Membrane Fusion

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