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. 2016 Oct;55(4):613-615.
doi: 10.1165/rcmb.2015-0387LE.

Persistent Pathology in Influenza-Infected Mouse Lungs

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Persistent Pathology in Influenza-Infected Mouse Lungs

Cindy M Kanegai et al. Am J Respir Cell Mol Biol. 2016 Oct.
No abstract available

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Figures

Figure 1.
Figure 1.
A murinized version of a pandemic H1N1 strain of influenza A (PR8) infection causes loss of alveolar epithelium and the expansion of keratin 5 (Krt5) pods. (A) Lineage-labeled type 2 alveolar epithelial cells (AEC2) and their progeny (red) are lost from large regions of the lung parenchyma of mice 7 days post-infection (dpi) with PR8. (B) Abundant Krt5+ “pods” (green) are observed in these regions devoid of normal alveolar epithelial lineages at 11 dpi. (C) The abundance of pro–surfactant-associated protein C (pro-SPC) is decreased concomitant with an increase in the abundance of KRT5 in the lungs of mice 11 dpi with PR8 compared with mice treated with saline or infected with X31. (D) Lineage-labeled AEC2 and their progeny are lost to a lesser extent 7 dpi X31 infection compared with PR8. (E) Krt5+ cells (green) are seen in the airways of mice 14 dpi with X31, but widespread pods are not seen in the distal lung. (F) 49 dpi with PR8, lineage-traced AEC2 (green) have given rise to RAGE (advanced glycosylation end product-specific receptor)+ AEC1 (white). In contrast, large adjacent regions of the lung are still devoid of unambiguous markers of AEC1 and AEC2, but still abnormally express K5 (red). (G) Magnified view of boxed region in F. (H, I) Section of wild-type lung 200 dpi with PR8 showing RAGE (white, AEC1) and K5 (red) in discrete regions. (J) Lineage traced K5+ cells (red) rarely give rise to RAGE+ AEC1 (white) 192 dpi with PR8. Nuclei were stained with 4′,6-diamidino-2-phenylindole (DAPI). Scale bars: 200 μm for panels A, B, D, and E. Scale bars: 100 μm for panels F, I, and J.

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