Punicalagin inhibits pro-inflammatory cytokines induced by influenza A virus

Introduction: Influenza A virus causes severe pneumonia in humans, leading to high morbidity and mortality. Studies have shown that an excessive immune response in overproduction of pro-inflammatory cytokines can exacerbate complications of influenza virus infection. Thus immune-targeted therapies are an appropriate strategy to control the disease. This study was conducted to investigate the effect of punicalagin on expression and concentration levels of tumor necrosis factor alpha (TNF alpha), interleukin 6 (IL-6) and interleukin1-beta in Madin-Darby Canine Kidney (MDCK) cells. Methods: In this experimental study, confluent MDCK cells were infected with influenza A virus (H1N1; PR8) and treated with punicalagin at different concentrations. After incubation, mRNA expression and concentration levels of TNF alpha, IL-6 and IL1-beta were investigated using real-time polymerase chain reaction (PCR) and enzyme-linked immunesorbent assay (ELISA), respectively. Results: The results of quantitative Real-time PCR showed a significant increase in TNF alpha, IL-6 and IL1-beta mRNA expression in control virus compared to cell control, and a significant, dose-dependent decrease in these expression levels in punicalagin-treated virus infected cells compared to control virus (P < 0.05). The ELISA results also confirmed the dose-dependent decrease in TNF alpha, IL-6 and IL1-beta concentrations in protein levels in punicalagin treated, virus infected cells compared to control virus (P < 0.05). Conclusions: Our results demonstrated the anti-inflammatory effects of punicalagin, and therefore suggests that the compound can be used as an appropriate treatment of choice to control cytokines-induced inflammation in influenza A virus infection.

Automated summary

Influenza A virus infection causes severe pneumonia, with an excessive immune response exacerbating complications. Punicalagin decreases the expression and concentration levels of tumor necrosis factor alpha, interleukin 6, and interleukin1-beta, exhibiting anti-inflammatory effects.