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. 2018 May;188(5):1149–1160. doi: 10.1016/j.ajpath.2018.01.021

Figure 2.

Figure 2

Alveolar epithelialization in diffuse alveolar injury with delayed epithelization case 1 versus control diffuse alveolar damage (DAD), matched in timing relative to the onset of clinical acute respiratory distress syndrome. A: Lung sections stained and examined at low magnification demonstrate diffuse alveolar injury and peribronchiolar basaloid pods (short arrows). Hyaline membranes are rare (long arrows, inset), and the lung interstitium is mildly thickened. B: Control case of DAD in the proliferative phase shows diffuse hyaline membranes (arrows, inset) and thickened lung interstitium. C: The absence of TTF1+/cytokeratin+ alveolar epithelium in case 1 is highlighted by the lack of cytokeratin cellular immunostaining; peribronchiolar basaloid pods are cytokeratin positive (arrows). D: In contrast, there is diffuse cytokeratin immunostaining of alveolar lining cells and hyaline membranes in the control. E: Denuded alveoli in case 1 show a lack of alveolar epithelium, with no hyaline membranes in this region. F and H: In control DAD, there are abundant CD163+ intra-alveolar and interstitial macrophages. G: CD163 immunohistochemistry demonstrates macrophages contiguously lining alveoli and in the interstitium. Original magnification: ×40 (A–D); ×200 (E–H); ×400 (insets). H&E, hematoxylin and eosin.