Respiratory viral infections drive different lung cytokine profiles in pigs.

backgroundSwine influenza A virus (IAV) and porcine reproductive and respiratory syndrome virus (PRRSV) are considered key viral pathogens involved in the porcine respiratory disease complex. Concerning the effect of one virus on another with respect to local immune response is still very limited. Determination of presence and quantity of cytokines in the lung tissue and its relation to the lung pathology can lead to a better understanding of the host inflammatory response and its influence on the lung pathology during single or multi-virus infection. The aim of the present study was to explore and compare the patterns of lung cytokine protein response in pigs after single or dual infection with swine IAV and/or PRRSV.

resultsInoculation with IAV alone causes an increase in lung concentration of IFN-α, IFN-ɣ, TNF-α, IL-6, IL-8 and IL-10, especially at 2 and 4 DPI. In PRRSV group, beyond early IFN-α, IFN-ɣ, IL-6, IL-8 and IL-10 induction, elevated levels of cytokines at 10 and 21 DPI have been found. In IAV+PRRSV inoculated pigs the lung concentrations of all cytokines were higher than in control pigs.

conclusionsCurrent results indicate that experimental infection of pigs with IAV or PRRSV alone and co-infection with both pathogens induce different kinetics of local cytokine response. Due to strong positive correlation between local TNF-α and IL-10 concentration and lung pathology, we hypothesize that these cytokines are involved in the induction of lung lesions during investigates infection. Nevertheless, no apparent increase in lung cytokine response was seen in pigs co-inoculated simultaneously with both pathogens compared to single inoculated groups. It may also explain no significant effect of co-infection on the lung pathology and pathogen load, compared to single infections. Strong correlation between local concentration of TNF-α, IFN-ɣ, IL-8 and SwH1N1 load in the lung, as well as TNF-α, IL-8 and PRRSV lung titres suggested that local replication of both viruses also influenced the local cytokine response during infection.