Tracheal tuft cells release ATP and link innate to adaptive immunity in pneumonia

Noran Abdel Wadood, Monika I. Hollenhorst, Mohamed Ibrahem Elhawy, Na Zhao, Clara Englisch, Saskia B. Evers, Mahana Sabachvili, Stephan Maxeiner, Amanda Wyatt, Christian Herr, Ann-Kathrin Burkhart, Elmar Krause, Daniela Yildiz, Anja Beckmann, Soumya Kusumakshi, Dieter Riethmacher, Markus Bischoff, Sandra Iden, Sören L. Becker, Brendan J. Canning, Veit Flockerzi, Thomas Gudermann, Vladimir Chubanov, Robert Bals, Carola Meier, Ulrich Boehm and Gabriela Krasteva-Christ ()
Additional contact information
Noran Abdel Wadood: Saarland University
Monika I. Hollenhorst: Saarland University
Mohamed Ibrahem Elhawy: Saarland University
Na Zhao: Saarland University
Clara Englisch: Saarland University
Saskia B. Evers: Saarland University
Mahana Sabachvili: Saarland University
Stephan Maxeiner: Saarland University
Amanda Wyatt: Saarland University
Christian Herr: Saarland University Hospital
Ann-Kathrin Burkhart: Saarland University
Elmar Krause: Saarland University
Daniela Yildiz: Saarland University
Anja Beckmann: Saarland University
Soumya Kusumakshi: Saarland University
Dieter Riethmacher: Nazarbayev University
Markus Bischoff: Saarland University
Sandra Iden: Saarland University
Sören L. Becker: Saarland University
Brendan J. Canning: The Johns Hopkins Asthma and Allergy Center
Veit Flockerzi: Saarland University
Thomas Gudermann: LMU Munich
Vladimir Chubanov: LMU Munich
Robert Bals: Saarland University
Carola Meier: Saarland University
Ulrich Boehm: Saarland University
Gabriela Krasteva-Christ: Saarland University

Nature Communications, 2025, vol. 16, issue 1, 1-17

Abstract: 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.

Date: 2025
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DOI: 10.1038/s41467-025-55936-5

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