Fig. 5
CXCL10 deficiency partially preserves alveolarization and lung matrix during regeneration from postnatal hyperoxia. A Experimental setup to study the role of CXCL10 in the regeneration phase after hyperoxia-induced lung injury: wildtype (WT) and Cxcl10 knockout (Cxcl10−/−) mice were exposed to normoxia (NOX, 21% O2) or hyperoxia (HYX, 85% O2) from birth until postnatal day 14 (P14); from P14 to P28, all mice were exposed to NOX. B Representative images of hematoxylin and eosin (H&E) stained lung tissue sections in mice at P28. C-E Quantitative histomorphometric analyses for the average surface area of a single alveolus (C), radial alveolar count (RAC; D), and septal thickness (E). F-I Representative images showing the spatial distribution of elastic fibers (Hart’s stain; F) and collagen (Picro-Sirius red stain; G) in mouse lungs at P28. Quantitative analyses of the elastic fiber (H) and collagen content (I) relative to lung tissue in percentage (%; elastic fiber and collagen fraction). Mean ± SEM; n = 3–6/group; Unpaired t test: $p < 0.05; Two-way ANOVA: *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001; scale bar: 20X, 100X