A Mechanism Study About Swine Influenza Virus Increasing Streptococcus Suis Serotype2Secondary Infection To The Procine Trachea Epithelial Cells And Procine Ateveolar Macrophage

Influenza virus (IFV) and respiratory bacteria (such as: S.pneumoniae，S.aureus，H.influenza) rank the most important pathogens affectiong human and animals today.Howevery, it is their ability to work together that presents the greatest threat to worldhealth. because co-infection with virus/bacteria are often observed in the field.Streptococcus suis serotype2is a major swine pathogen that is able to infect thecells from the upper respiratory tract, which causing pneumonia, meningitis,arthritis, sepsis in pig. In a total of35serotypes, serotype2is most virulent serotypeand the easist be isolated in the infected pigs.The hypothesis of the present study was that SIV pre-infection of respiratoryepithelial cells or alveolar macropahge facilitates a secondary infection with S. suisserotype2. Finally, it is the first time to demonstrate SIV pre-infection increasingS.suis type2encapsulated strain secondary infection. In this study, using a CanadianH1N1SIV strain and S. suis strains and a newborn pig tracheal cell line or primaryporcine alveolar macrophage to construct co-infection model, we observed up to100times increasing in bacterial adhesion, invasion/pahgocytosis of virus-infected cellscompared with normal cells. This enhancement of bacterial adhesion/invasion couldbe inhibited by the specific viral antibody and bacterial capsular polysaccharide (CPS)which contains Sialic acid. And non-encapsulated mutant strain did not show anypromotion in adhesion/invasion to virus-infected cells; well encapsulated S. suisserotype2(but not a non-encapsulated mutant) was able to inhibit thehaemagglutination between SIV and red blood cells. Binding of bacterial capsularsialic acid to viral hemagglutinin (HA) was suspected when purified native (but notdesialylated) S. suis serotype2CPS significantly inhibited bacteria and virus-infectedcell interactions. In addition, increased bacterial adhesion/invasion was observed withserotypes possessing sialic-acid rich CPS only. Using quantitative RT-PCR, we alsoshowed that the expression of several pro-inflammatory cytokines was significantly enhanced in cells dually infected with SIV and S. suis.Overall, our results is the first time report about specific binding of a sialic acidmoiety of a bacterial CPS to the HA of influenza virus. In this specific case, thisbinding would enhance S. suis serotype2adhesion, invasion and inflammatoryresponse of virus-pre-infected respiratory epithelial cells and alveolar macrophage. Anamplified interaction of S. suis with respiratory epithelial cells or alveolar macrophagemay play an important role in both, pneumonia and systemic disease caused by thisimportant pathogen.