Taurolidine resists pulmonary artery vasoconstriction induced by influenza virus infection via inhibiting Ca 2+ influx and MLCK/p-MLC signaling pathway

Abstract Background Influenza virus causes worldwide outbreaks and seasonal epidemics, severely threatening public health and social development. Effective prevention and therapy for influenza infections are a major challenge to global healthcare. Results Taurolidine effectively inhibited the proliferation of several human or animal influenza virus strains and protected mice from lethal-infection. Taurolidine treatment decreased the viral titer in the lungs of infected mice, reduced immune cells infiltration, and alleviated lung pathology. Additionally, influenza virus infection increased blood pressure, pulse wave velocity, and pulmonary aortic thickness in mouse model, as well as promoted the increase of intracellular Ca²⁺ concentration and pulmonary artery vasoconstriction. These effects were attenuated by taurolidine treatment through inhibiting the activation of the MLCK/p-MLC pathway. Conclusions These findings confirm the effectiveness of taurolidine as an antiviral agent and highlight its important roles in host immune cell infiltration and vasoconstriction induced by influenza virus infection.