tetano
Editor, Senior Moderator
Sci Rep
. 2024 Sep 12;14(1):21324.
doi: 10.1038/s41598-024-72115-6. Influenza induces lung lymphangiogenesis independent of YAP/TAZ activity in lymphatic endothelial cells
Erin Crossey[SUP] #[/SUP][SUP] 1 [/SUP], Senegal Carty[SUP] #[/SUP][SUP] 2 [/SUP], Fengzhi Shao[SUP] 2 [/SUP], Jhonatan Henao-Vasquez[SUP] 2 [/SUP], Alexandra B Ysasi[SUP] 2 [/SUP], Michelle Zeng[SUP] 2 [/SUP], Anne Hinds[SUP] 2 [/SUP], Ming Lo[SUP] 3 4 [/SUP], Andrew Tilston-Lunel[SUP] 5 [/SUP], Xaralabos Varelas[SUP] 5 [/SUP], Matthew R Jones[SUP] 2 [/SUP], Alan Fine[SUP] 2 [/SUP]
Affiliations
The lymphatic system consists of a vessel network lined by specialized lymphatic endothelial cells (LECs) that are responsible for tissue fluid homeostasis and immune cell trafficking. The mechanisms for organ-specific LEC responses to environmental cues are not well understood. We found robust lymphangiogenesis during influenza A virus infection in the adult mouse lung. We show that the number of LECs increases twofold at 7 days post-influenza infection (dpi) and threefold at 21 dpi, and that lymphangiogenesis is preceded by lymphatic dilation. We also show that the expanded lymphatic network enhances fluid drainage to mediastinal lymph nodes. Using EdU labeling, we found that a significantly higher number of pulmonary LECs are proliferating at 7 dpi compared to LECs in homeostatic conditions. Lineage tracing during influenza indicates that new pulmonary LECs are derived from preexisting LECs rather than non-LEC progenitors. Lastly, using a conditional LEC-specific YAP/TAZ knockout model, we established that lymphangiogenesis, fluid transport and the immune response to influenza are independent of YAP/TAZ activity in LECs. These findings were unexpected, as they indicate that YAP/TAZ signaling is not crucial for these processes.
. 2024 Sep 12;14(1):21324.
doi: 10.1038/s41598-024-72115-6. Influenza induces lung lymphangiogenesis independent of YAP/TAZ activity in lymphatic endothelial cells
Erin Crossey[SUP] #[/SUP][SUP] 1 [/SUP], Senegal Carty[SUP] #[/SUP][SUP] 2 [/SUP], Fengzhi Shao[SUP] 2 [/SUP], Jhonatan Henao-Vasquez[SUP] 2 [/SUP], Alexandra B Ysasi[SUP] 2 [/SUP], Michelle Zeng[SUP] 2 [/SUP], Anne Hinds[SUP] 2 [/SUP], Ming Lo[SUP] 3 4 [/SUP], Andrew Tilston-Lunel[SUP] 5 [/SUP], Xaralabos Varelas[SUP] 5 [/SUP], Matthew R Jones[SUP] 2 [/SUP], Alan Fine[SUP] 2 [/SUP]
Affiliations
- PMID: 39266641
- DOI: 10.1038/s41598-024-72115-6
The lymphatic system consists of a vessel network lined by specialized lymphatic endothelial cells (LECs) that are responsible for tissue fluid homeostasis and immune cell trafficking. The mechanisms for organ-specific LEC responses to environmental cues are not well understood. We found robust lymphangiogenesis during influenza A virus infection in the adult mouse lung. We show that the number of LECs increases twofold at 7 days post-influenza infection (dpi) and threefold at 21 dpi, and that lymphangiogenesis is preceded by lymphatic dilation. We also show that the expanded lymphatic network enhances fluid drainage to mediastinal lymph nodes. Using EdU labeling, we found that a significantly higher number of pulmonary LECs are proliferating at 7 dpi compared to LECs in homeostatic conditions. Lineage tracing during influenza indicates that new pulmonary LECs are derived from preexisting LECs rather than non-LEC progenitors. Lastly, using a conditional LEC-specific YAP/TAZ knockout model, we established that lymphangiogenesis, fluid transport and the immune response to influenza are independent of YAP/TAZ activity in LECs. These findings were unexpected, as they indicate that YAP/TAZ signaling is not crucial for these processes.