Figure 3
IL-6 deficiency results in insufficient neutrophils in the lung during influenza H1N1 virus infection and inability to clear the virus. (a) Virus titers determined by the number of influenza polymerase A (PA) RNA copies by real-time RT-PCR in total lung of WT and IL-6 KO mice (n=5) at different days p.i. with the H1N1 PR8 virus (3 × 103 EIU). (b) Percentage of CD8 T cells that were positive for nucleoprotein (NP) tetramers within the mediastinal lymph node from WT and IL-6 KO mice (n=4) 9 days p.i., as determined by flow cytometry analysis. (c–f) Percentage (panels c and e) and total number (panels d and f) of macrophages (panels c and d) and neutrophils (panels e and f) in BAL from WT and IL-6 KO mice (n=5) at different days p.i. with the H1N1 PR8 virus. (g) Virus titers determined by the number of influenza PA RNA copies in the total lung and in cells from BAL of WT mice (n=4) 5 days p.i. with PR8 virus. (h) Kaplan–Meier survival curve of WT mice (n=5) infected with the H1N1 PR8 virus that received an intraperitoneal administration (500 μg per mouse) of an anti-Ly6G Ab or an isotype control 1 day before infection and another administration at day 3 p.i. *P<0.05. NS denotes not significant. Statistical significance was determined by two-way ANOVA (panels a, c–f), Student's t-test (panels b and g), or log-rank test (panel h). Results are representative of two to four independent experiments. ANOVA, analysis of variance; BAL, bronchoalveolar lavage; IL, interleukin; KO, knockout; p.i., post infection; RT-PCR, reverse transcription-PCR; WT, wild type.
