1. Tracheal tuft cells release ATP and link innate to adaptive immunity in pneumonia.
- Author
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Abdel Wadood, Noran, Hollenhorst, Monika I., Elhawy, Mohamed Ibrahem, Zhao, Na, Englisch, Clara, Evers, Saskia B., Sabachvili, Mahana, Maxeiner, Stephan, Wyatt, Amanda, Herr, Christian, Burkhart, Ann-Kathrin, Krause, Elmar, Yildiz, Daniela, Beckmann, Anja, Kusumakshi, Soumya, Riethmacher, Dieter, Bischoff, Markus, Iden, Sandra, Becker, Sören L., and Canning, Brendan J.
- Abstract
Tracheal tuft cells shape immune responses in the airways. While some of these effects have been attributed to differential release of either acetylcholine, leukotriene C4 and/or interleukin-25 depending on the activating stimuli, tuft cell-dependent mechanisms underlying the recruitment and activation of immune cells are incompletely understood. Here we show that Pseudomonas aeruginosa infection activates mouse tuft cells, which release ATP via pannexin 1 channels. Taste signaling through the Trpm5 channel is essential for bacterial tuft cell activation and ATP release. We demonstrate that activated tuft cells recruit dendritic cells to the trachea and lung. ATP released by tuft cells initiates dendritic cell activation, phagocytosis and migration. Tuft cell stimulation also involves an adaptive immune response through recruitment of IL-17A secreting T helper cells. Collectively, the results provide a molecular framework defining tuft cell dependent regulation of both innate and adaptive immune responses in the airways to combat bacterial infection.Tracheal tuft cells have been shown to facilitate the recruitment of immune cells during infection of the airways. Here the authors show that P. aeruginosa lung infection in mice activates tuft cells to release ATP which subsequently activates DC and promotes IL-17A secreting T cells. [ABSTRACT FROM AUTHOR]
- Published
- 2025
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