Fig. 6
From: C3a receptor antagonism as a novel therapeutic target for chronic rhinosinusitis
Complement C3a receptor deficiency or therapeutic antagonism reduce sinonasal inflammation and epithelial remodeling. Hematoxylin-stained and eosin-stained sections of sinus mucosa from animals in each treatment group. Note the extensive sub-epithelial inflammation characterized by eosinophil, macrophage, and neutrophil infiltrates in Af-challenged mice as compared to control, C3aR−/− and treatment groups (arrows). Further note the more pronounced mucus-producing cells lining the sinus lumen (*). Images representative of n = 6 in each group, scale as shown
