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Transcriptional approach to study porcine tracheal epithelial cells individually or dually infected with swine influenza virus and Streptococcus suis.

Dang Y, Lachance C, Wang Y, Gagnon CA, Savard C, Segura M, Grenier D, Gottschalk M - BMC Vet. Res. (2014)

Bottom Line: Outbreaks of swine influenza virus with a significant level of co-infections due to S. suis have lately been reported.In a co-infection situation, although these cells would be 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 proinflammatory mediators during a co-infection with influenza virus may be important in the pathogenesis and clinical outcome of S. suis-induced respiratory diseases.

View Article: PubMed Central - HTML - PubMed

Affiliation: Faculté de Médecine Vétérinaire, Université de Montréal, 3200 Sicotte, St-Hyacinthe, J2S 2M2 Québec, Canada. marcelo.gottschalk@umontreal.ca.

ABSTRACT

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, for the first time, the transcriptional host response of swine tracheal epithelial (NPTr) cells to H1N1 swine influenza virus (swH1N1) infection, S. suis serotype 2 infection and a dual infection, we carried out a comprehensive gene expression profiling using a microarray approach.

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 resulted in fewer 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 compared to infection with each pathogen individually. This synergy may be the consequence, at least in part, of an increased bacterial adhesion/invasion of epithelial cells previously infected by swH1N1, as recently reported.

Conclusion: Influenza virus would replicate in the respiratory epithelium and induce an inflammatory infiltrate comprised of mononuclear cells and neutrophils. In a co-infection situation, although these cells would be 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 proinflammatory mediators during a co-infection with influenza virus may be important in the pathogenesis and clinical outcome of S. suis-induced respiratory diseases.

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Proinflammatory cytokine and chemokine genes are highly expressed in NPTr epithelial cells infected by S. suis and swine influenza virus. Expression of TNF, IFN-β, IFNλ1, IL-1, IL-6, IL-8, VCAM-1, CCL5, PLAU, and COX-2 genes in NPTr cells infected with S. suis, H1N1, or S. suis/H1N1 when compared to mock-infected cells, as quantified by qPCR assay. Data represent mean relative expression values of mRNA ± SEM. Groups that are significantly different are indicated by different letters (a, b, and c), as determined by One-way ANOVA with p ≤ 0.05.
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Figure 4: Proinflammatory cytokine and chemokine genes are highly expressed in NPTr epithelial cells infected by S. suis and swine influenza virus. Expression of TNF, IFN-β, IFNλ1, IL-1, IL-6, IL-8, VCAM-1, CCL5, PLAU, and COX-2 genes in NPTr cells infected with S. suis, H1N1, or S. suis/H1N1 when compared to mock-infected cells, as quantified by qPCR assay. Data represent mean relative expression values of mRNA ± SEM. Groups that are significantly different are indicated by different letters (a, b, and c), as determined by One-way ANOVA with p ≤ 0.05.

Mentions: In order not only to validate microarray results but also to further study some specific genes based on their potential implication in immune and inflammatory response processes, we carried out quantitative real-time PCR (qPCR) on 13 different genes (Additional file1: Table S3). All tested genes presented a perfect correlation with microarray results, with the exception of TNF. This proinflammatory cytokine did not show any significant difference by microarray, but its expression was shown to be up-regulated for virus and co-infected cells (Figure 4). A higher sensitivity of the qPCR assay can explain this difference.


Transcriptional approach to study porcine tracheal epithelial cells individually or dually infected with swine influenza virus and Streptococcus suis.

Dang Y, Lachance C, Wang Y, Gagnon CA, Savard C, Segura M, Grenier D, Gottschalk M - BMC Vet. Res. (2014)

Proinflammatory cytokine and chemokine genes are highly expressed in NPTr epithelial cells infected by S. suis and swine influenza virus. Expression of TNF, IFN-β, IFNλ1, IL-1, IL-6, IL-8, VCAM-1, CCL5, PLAU, and COX-2 genes in NPTr cells infected with S. suis, H1N1, or S. suis/H1N1 when compared to mock-infected cells, as quantified by qPCR assay. Data represent mean relative expression values of mRNA ± SEM. Groups that are significantly different are indicated by different letters (a, b, and c), as determined by One-way ANOVA with p ≤ 0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4022123&req=5

Figure 4: Proinflammatory cytokine and chemokine genes are highly expressed in NPTr epithelial cells infected by S. suis and swine influenza virus. Expression of TNF, IFN-β, IFNλ1, IL-1, IL-6, IL-8, VCAM-1, CCL5, PLAU, and COX-2 genes in NPTr cells infected with S. suis, H1N1, or S. suis/H1N1 when compared to mock-infected cells, as quantified by qPCR assay. Data represent mean relative expression values of mRNA ± SEM. Groups that are significantly different are indicated by different letters (a, b, and c), as determined by One-way ANOVA with p ≤ 0.05.
Mentions: In order not only to validate microarray results but also to further study some specific genes based on their potential implication in immune and inflammatory response processes, we carried out quantitative real-time PCR (qPCR) on 13 different genes (Additional file1: Table S3). All tested genes presented a perfect correlation with microarray results, with the exception of TNF. This proinflammatory cytokine did not show any significant difference by microarray, but its expression was shown to be up-regulated for virus and co-infected cells (Figure 4). A higher sensitivity of the qPCR assay can explain this difference.

Bottom Line: Outbreaks of swine influenza virus with a significant level of co-infections due to S. suis have lately been reported.In a co-infection situation, although these cells would be 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 proinflammatory mediators during a co-infection with influenza virus may be important in the pathogenesis and clinical outcome of S. suis-induced respiratory diseases.

View Article: PubMed Central - HTML - PubMed

Affiliation: Faculté de Médecine Vétérinaire, Université de Montréal, 3200 Sicotte, St-Hyacinthe, J2S 2M2 Québec, Canada. marcelo.gottschalk@umontreal.ca.

ABSTRACT

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, for the first time, the transcriptional host response of swine tracheal epithelial (NPTr) cells to H1N1 swine influenza virus (swH1N1) infection, S. suis serotype 2 infection and a dual infection, we carried out a comprehensive gene expression profiling using a microarray approach.

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 resulted in fewer 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 compared to infection with each pathogen individually. This synergy may be the consequence, at least in part, of an increased bacterial adhesion/invasion of epithelial cells previously infected by swH1N1, as recently reported.

Conclusion: Influenza virus would replicate in the respiratory epithelium and induce an inflammatory infiltrate comprised of mononuclear cells and neutrophils. In a co-infection situation, although these cells would be 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 proinflammatory mediators during a co-infection with influenza virus may be important in the pathogenesis and clinical outcome of S. suis-induced respiratory diseases.

Show MeSH
Related in: MedlinePlus