Abstract
Mice were infected with influenza and treated with a CXCR2 antagonist in combination with antiviral or antiviral alone starting 4 days postinfection. Neutrophil recruitment to the lung was reduced, and improvements in health outcomes and lung consolidation were observed in combination-treated mice with no evidence of worsening outcome.
Highlights
Mice were infected with influenza and treated with a CXCR2 antagonist in combination with antiviral or antiviral alone starting 4 days postinfection
Respiratory neutrophil levels and their associated chemokines involved in recruitment to sites of inflammation are correlated with clinical symptom severity of influenza infection in humans, in particular in those who died [4, 5]
We demonstrated that attenuation of neutrophil recruitment to the lungs by therapeutic treatment with the CXCR2 antagonist SB-332235Z together with oseltamivir phosphate (OSV) improved outcomes in a model of severe influenza infection, with no evidence of worsening outcome
Summary
Mice were infected with influenza and treated with a CXCR2 antagonist in combination with antiviral or antiviral alone starting 4 days postinfection. Despite the availability of vaccines and direct-acting antiviral (DAA) drugs, influenza continues to cause severe disease and remains a significant burden on the global healthcare system [1]. DAA agents are able to reduce viral load, they need to be given early in the course of disease to have an effect and have not prevented death in patients with severe influenza [2]. Pathogenesis of influenza results from direct viral cytopathology and from an overzealous host immune response, leading to lung inflammation and decreases in lung function. We explored the ability of the CXCR2 antagonist SB-332235Z to reduce excessive neutrophil accumulation and subsequent inflammatory damage in the lungs of influenza-infected mice
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