Fig. 7
From: Cathelicidins prime platelets to mediate arterial thrombosis and tissue inflammation
Cathelicidins promote lung injury. a, b Representative histology images of lung tissue obtained from patients with acute pneumonia and two control subjects without tissue inflammation. Patient 1 presented with aspiration pneumonia. Immunohistochemistry for LL-37 (a, b) and hematoxylin-eosin (H&E) staining (b). Bars, 100 µm (a) or 50 µm (b). c–t Mouse model of acute lung injury (ALI) induced by intratracheal injection of 0.1 M HCl. c Representative images of H&E stained mouse lung tissue after ALI in wild type and CRAMP−/− mice. Bar, 50 µm. d Alveolar neutrophil counts, e number of interstitial (including pulmonary intravascular) neutrophils, and f alveolar permeability after ALI in wild type (n = 6) and CRAMP−/− mice (n = 7). g Alveolar neutrophils and h interstitial (including pulmonary intravascular) neutrophils after ALI in wild type (wt → wt) and CRAMP−/− (ko → wt) chimeras (n = 7). i–k Analysis of citrullinated histone H3 (citH3) staining in Ly6G+ neutrophils. i Representative image of lung tissue after ALI. CitH3 (green), Ly6G (red), DAPI (nuclear stain, blue). Bar, 10 µm. j, k Quantification of citH3 staining in Ly6G+ neutrophils (n = 6). l Alveolar permeability after ALI (n = 7). m, n Flow cytometry analysis of platelet–neutrophil aggregates after ALI in m systemic circulation (n = 6) and n the pulmonary vascular compartment (n = 7). o–r Flow cytometry analysis of o P-selectin surface expression, p GPIIb/IIIa activation, q HMGB1 surface expression, and r phosphatidylserine (PS) exposure on platelets. s Survival curves and t oxygen saturations after 30 min after ALI induction (n = 6). Graphs show mean and SEM. P-values were determined by Mann–Whitney U-test (d, f, g, h, l, n), unpaired t-test (e, j, k, m, o, p, q, r, t), or Log-rank (Mantel-Cox) test (s)
