To investigate the role of interleukin-1 receptor type 1 (IL-1R1) signaling in H1N1 influenza virus infection.

IL-1R1 knockout (IL-1R1^-/-) mice and wild type (WT) mice were infected intranasally with 2×10⁴ TCID₅₀ (50% tissue culture infective dose) of influenza virus H1N1 PR8. Changes in clinical signs, survivals and bodyweights of those mice were monitored daily for 14 consecutive days. Three mice from each group were sacrificed at 3, 7 and 14 days post infection (d.p.i), from which whole lungs were harvested. A part of the lobes was fixed in 4% paraformaldehyde for histopathological assessment and the rest were split and stored at -80 centigrade for further analysis. Real-time quantitative PCR and cytometric bead array (CBA) were performed to detect viral loads in lungs and inflammatory cytokines in supernatants of lung homogenates.

The mice in both groups showed severe symptoms after the infection of PR8. The maximum bodyweight loss of IL-1R1^-/- mice [(24.22±0.80) % at 8 d. p.i] was lower than that of WT mice [(28.03±1.51)% at 9 d. p.i] (P<0.05). The IL-1R1^-/- mice with PR8 infection showed a higher survival rate (90%) as compared with that of the control group (40%) (P<0.05). No statistical differences in virus loads were observed between the two groups at 3, 7 and 14 d. p.i. The lung weight to body weight ratio of IL-1R1^-/- mice [(1.42±0.03) %] was lower than that of WT mice [(1.79±0.08) %] at 3 d. p.i (P<0.05). Pathological changes in IL-1R1^-/- mice were less severe than those in WT mice. CBA detection assay revealed that the proinflammatory cytokines in lungs of IL-1R1^-/- mice were less than those in WT mice.

IL-1R1 signaling plays a pathogenic role in mice infected with 2×10⁴ TCID₅₀ of influenza virus PR8 by promoting inflammatory responses.

IL-1R1; Influenza virus; Inflammatory responses