Fig. 6.
IL-6 deficiency promotes eosinophilic airway inflammation but does not reduce methacholine hyperresponsiveness in the complete Freund’s adjuvant and house dust mite antigen (CFA/HDM) model of severe asthma. Wild-type mice were naive or subjected to the CFA/HDM model of severe asthma. IL-6- or IL-6 receptor (IL-6R)-deficient mice were subjected to the CFA/HDM model of severe asthma. Total cells (A), macrophages (B), lymphocytes (C), eosinophils (D), and neutrophils (E) were measured from bronchoalveolar lavage (BAL). n = 4 or 11 mice/group (A–E). IL-6 (F), IL-17A (G), IFNγ (H), IL-4 (I), IL-5 (J), and IL-13 (K) were measured from BAL. n = 4 mice/group (F–K). *P ≤ 0.05, **P ≤ 0.01, and ***P ≤ 0.001 compared with CFA/HDM (A–K). IL-5 (L), IL-13 (M), IL-17A (N), and IFNγ (O) were measured from HDM-restimulated mediastinal lymph node (MLN) cell culture supernatants. Serum amyloid A 1/2 was measured from BAL (P) and serum (Q). n = 4 mice/group (L–Q). *P ≤ 0.05, **P ≤ 0.01, and ****P ≤ 0.0001 compared with CFA/HDM. Airway resistance (RN; R), tissue damping (G; S), and tissue elastance H; T) were measured. n = 8 or 10 mice/group (R–T). *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001, and ****P ≤ 0.0001 compared with naive. #P ≤ 0.05 compared with CFA/HDM.