Fig. 4.

CL27c maintains normal lung architecture and function in the model of OVA-induced chronic allergic asthma. a Hematoxylin and eosin staining of lung sections in control and OVA-treated mice further receiving either CL27c (2 mg/ml) or Dexamethasone (5 mg/kg). Bar = 25 μm. b Histopathological changes in lung inflammation, scored as described in Methods, in control (OVA−) and OVA-treated (OVA+) mice further receiving either CL27c or Dexamethasone (Dexa) (from left to right, airways n = 5, 8, 7, 8, vasculature n = 5, 8, 7, 8, parenchyma n = 5, 8, 7, 8, and overall n = 5, 8, 7, 8 independent experiments, respectively). c Representative Masson’s trichrome staining showing areas of fibrosis (blue-staining) in the OVA group. Bar = 100 μm. d Quantification of fibrosis confirming the antifibrotic effect of either CL27c or Dexamethasone (from left to right n = 5, 7, 5, 6, independent experiments, respectively). e Analysis of Lung Resistance (RL) (form left to right n = 5, 8, 6, 6 independent experiments, respectively) and f dynamic compliance (Cdyn) (from left to right n = n = 6, 8, 7, 6 independent experiments, respectively) in mice with chronic asthma. Results represent mean ± s.e.m., *P < 0.05, **P < 0.01, ***P < 0.001 determined using either Kruskal–Wallis followed by Dunn’s test (b) or one-way ANOVA followed by Bonferroni post-hoc test (d–f). n.s. = non-significant (P > 0.05)