IL-17 receptor-deficient mice have increased resistance to otherwise lethal influenza infection (96.14)

Abstract

Abstract IL-17 is a CD4+ T cell-derived cytokine that has been previously been shown to play a role in the immune response to several different lung infections. Specifically, it has been shown to induce neutrophil recruitment and inflammation in response to a variety of pathogens, including Pseudomonas aeruginosa, Klebsiella pneumoniae, and Mycoplasma pneumoniae. Additionally, it has been shown that IL-17 is upregulated in respiratory syncitial virus (RSV) infection, but its role in other viral pulmonary infections remains poorly described. In order to investigate the role of IL-17 in influenza infections, BALB/c mice lacking the IL-17 receptor were challenged intranasally with a lethal dose of influenza A/Puerto Rico/8/34 (H1N1). The mice were monitored for weight loss and signs of clinical illness on a daily basis. When compared to BALB/c controls, the IL-17 receptor knockout mice exhibited delayed weight loss and had higher survival rates. Additionally, the control mice exhibited higher levels of protein and lactate dehydrogenase in the BAL fluid, markers of acute lung injury, during the course of infection. These data suggest that the effects of IL-17R signaling contributes to lung injury and the pathology of a lethal influenza infection in a murine model.