tetano
Editor, Senior Moderator
Am J Physiol Lung Cell Mol Physiol. 2019 Mar 25. doi: 10.1152/ajplung.00032.2019. [Epub ahead of print]
[h=1]Development of solitary chemosensory cells in the distal lung after severe influenza injury.[/h] Rane CK[SUP]1[/SUP], Jackson SR[SUP]1[/SUP], Pastore CF[SUP]1[/SUP], Zhao G[SUP]1[/SUP], Weiner AI[SUP]1[/SUP], Patel NN[SUP]2[/SUP], Herbert DR[SUP]1[/SUP], Cohen NA[SUP]3[/SUP], Vaughan AE[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] H1N1 influenza virus infection induces dramatic and permanent alveolar remodeling mediated by p63+ progenitor cell expansion in both mice and some patients with acute respiratory distress syndrome. This persistent lung epithelial dysplasia is accompanied by chronic inflammation, but the driver(s) of this pathology are unknown. This work identified de novo appearance of solitary chemosensory cells (SCCs), as defined by the tuft cell marker DCLK1, in post-influenza lungs arising in close proximity with the dysplastic epithelium, whereas uninjured lungs are devoid of SCCs. Interestingly, fate mapping demonstrated that these cells are derived from p63-expressing lineage negative progenitors, the same cell-of-origin as the dysplastic epithelium. Direct activation of SCCs with denatonium and succinate increased plasma extravasation specifically in post-influenza virus-injured lungs. Thus, we demonstrate the previously unrecognized development and activity of SCCs in the lung following influenza virus infection, implicating SCCs as a central feature of dysplastic remodeling.
[h=4]KEYWORDS:[/h] chemosensory; inflammation; influenza; progenitor; tuft
PMID: 30908939 DOI: 10.1152/ajplung.00032.2019
[h=1]Development of solitary chemosensory cells in the distal lung after severe influenza injury.[/h] Rane CK[SUP]1[/SUP], Jackson SR[SUP]1[/SUP], Pastore CF[SUP]1[/SUP], Zhao G[SUP]1[/SUP], Weiner AI[SUP]1[/SUP], Patel NN[SUP]2[/SUP], Herbert DR[SUP]1[/SUP], Cohen NA[SUP]3[/SUP], Vaughan AE[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] H1N1 influenza virus infection induces dramatic and permanent alveolar remodeling mediated by p63+ progenitor cell expansion in both mice and some patients with acute respiratory distress syndrome. This persistent lung epithelial dysplasia is accompanied by chronic inflammation, but the driver(s) of this pathology are unknown. This work identified de novo appearance of solitary chemosensory cells (SCCs), as defined by the tuft cell marker DCLK1, in post-influenza lungs arising in close proximity with the dysplastic epithelium, whereas uninjured lungs are devoid of SCCs. Interestingly, fate mapping demonstrated that these cells are derived from p63-expressing lineage negative progenitors, the same cell-of-origin as the dysplastic epithelium. Direct activation of SCCs with denatonium and succinate increased plasma extravasation specifically in post-influenza virus-injured lungs. Thus, we demonstrate the previously unrecognized development and activity of SCCs in the lung following influenza virus infection, implicating SCCs as a central feature of dysplastic remodeling.
[h=4]KEYWORDS:[/h] chemosensory; inflammation; influenza; progenitor; tuft
PMID: 30908939 DOI: 10.1152/ajplung.00032.2019