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Fig. 1 | Critical Care

Fig. 1

From: Interleukin-34: an important modifier in the pathogenesis of influenza pneumonia

Fig. 1Fig. 1

Increased IL-34 production contributed to morbidity and mortality after influenza virus infection. a IL-34 concentrations were assessed by ELISA in serum samples collected from 22 H1N1-infected patients upon hospital admission and from 22 healthy age- and gender-matched healthy controls. Horizontal bars represent median values, and dots represent individual participants. P < 0.05 when compared to healthy controls (Mann–Whitney U test). b Serum IL-34 levels in severe cases of influenza patients (n = 7) and mild cases of influenza patients (n = 15). P < 0.05 when compared to mild patients (Mann–Whitney U test). c Serum concentrations of IL-34 in influenza patients (n = 8) in the acute and recovery phases. P < 0.05 when compared to recovered patients (Wilcoxon signed-rank test). d C57BL/6Je mice (n = 5 per group) were infected intranasally with influenza virus PR8 (20 TCID50), and lungs and blood were collected on day 1, 2, or 3 after viral infection. Samples were assayed for IL-34 concentrations by ELISA. P < 0.05 when compared to mock controls (Kruskal–Wallis test followed by Dunn's multiple comparisons post test). e C57BL/6Je mice were intranasally infected with a lethal dose of influenza PR8 (90 TCID50). At 2 h post infection, mice were injected with 10 μg of sheep anti-mouse IL-34 antibody, followed by booster doses of 5 μg on day 2 and 4. Sheep IgG was used as a control. Weight changes of mice (n = 20 per group) after lethal influenza infection were calculated. P < 0.05 when compared to mice treated with IgG control (Mann–Whitney U test). f Survival rate was assessed daily following lethal influenza virus infection. Each group consisted of 20 mice treated with or without IL-34 blockade. Kaplan–Meier survival curves were shown and significance was determined using the log-rank test. P < 0.05 when compared to mice treated with IgG control (log-rank survival test). g In parallel, cohorts of infected mice (n = 5 per group) were sacrificed at day 5 after lethal influenza virus infection for measurement of virus titers in the lung, and no statistical significance was observed using Mann–Whitney U test. h The lung injury scores of lung sections from infected mice at day 5 after lethal influenza virus infection were evaluated (n = 5 per group). Lung injury scoring system parameters include the presence of neutrophils in the alveolar space, neutrophils in the interstitial space, hyaline membranes, proteinaceous debris filling the airspaces and alveolar septal thickening. At least 20 random regions were scored 0–2 independently and the final lung injury score was calculated. P < 0.05 when compared to mice treated with IgG control (Mann–Whitney U test). i C57BL/6Je mice were intranasally infected with a non-lethal dose of influenza PR8 (20 TCID50). Immediately after viral infection, mice were injected with 2 μg of recombinant mouse IL-34 protein through tail vein injection. PBS was used as saline control. Weight changes of mice (n = 20 per group) after non-lethal influenza infection were calculated. P < 0.05 when compared to mice treated with saline control (Mann–Whitney U test). j Survival rate was assessed daily following non-lethal influenza virus infection. Each group consisted of 20 mice treated with or without recombinant IL-34 protein. Kaplan–Meier survival curves were shown and significance was determined using the log-rank test. P < 0.05 when compared to mice treated with saline control (log-rank survival test). k In parallel, cohorts of infected mice (n = 5 per group) were sacrificed at day 5 after non-lethal influenza virus infection for measurement of virus titers in the lung, and no statistical significance was observed using Mann–Whitney U test. l The lung injury scores of lung sections from infected mice at day 5 after non-lethal influenza virus infection were evaluated (n = 5 per group). P < 0.05 when compared to mice treated with saline control (Mann–Whitney U test)

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