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. 2017 Oct 27;73(6):546–556. doi: 10.1136/thoraxjnl-2017-210010

Figure 5.

Figure 5

Neutrophil-derived mCRAMP activates the inflammasome in alveolar macrophages during influenza infection. Mice were administered neutrophil-depleting (1A8) or control (2A3) antibody intraperitoneally and inoculated with influenza or PBS intranasally and culled 24 hours later. (A) Amounts of mCRAMP in the BALF were determined by Western blot (representative image from two experiments depicted). (B) Densitometry analysis of mCRAMP expression from Western blot. Correlation between mCRAMP (values from densitometry analysis) and (C) airway neutrophil or (D) BALF IL-1β at 24 hours post infection. Influenza/2A3 group are depicted as closed symbols and influenza/1A8 as open symbols. (E) Alveolar macrophages or (F) bone marrow neutrophils were primed with imiquimod (IM) for 4 hours followed by stimulation with mCRAMP for 2 hours and ensuing IL-1β release into supernatant assessed by ELISA. The graphs present (B) data combined from two experiments with at least five mice per group; (C, D) Spearman correlation from two experiments with at least five mice per group; (E) data combined from two experiments with n=2 per group or (F) one experiment with n=4 per group. Results are depicted as median±IQR. p Values were calculated using Mann-Whitney statistical test (B) or Kruskal-Wallis with Dunn’s post-test (E and F).