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Wagner, C.* ; Uliczka, K.* ; Bossen, J.* ; Niu, X.* ; Fink, C.* ; Thiedmann, M.* ; Knop, M.* ; Vock, C.* ; Abdelsadik, A.* ; Zissler, U.M. ; Isermann, K.* ; Garn, H.* ; Pieper, M.* ; Wegmann, M.* ; Koczulla, A.R.* ; Vogelmeier, C.F.* ; Schmidt-Weber, C.B. ; Fehrenbach, H.* ; König, P.* ; Silverman, N.* ; Renz, H.* ; Pfefferle, P.I.* ; Heine, H.* ; Roeder, T.*

Constitutive immune activity promotes JNK- and FoxO-dependent remodeling of Drosophila airways.

Cell Rep. 35:108956 (2021)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Extensive remodeling of the airways is a major characteristic of chronic inflammatory lung diseases such as asthma or chronic obstructive pulmonary disease (COPD). To elucidate the importance of a deregulated immune response in the airways for remodeling processes, we established a matching Drosophila model. Here, triggering the Imd (immune deficiency) pathway in tracheal cells induced organ-wide remodeling. This structural remodeling comprises disorganization of epithelial structures and comprehensive epithelial thickening. We show that these structural changes do not depend on the Imd pathway's canonical branch terminating on nuclear factor κB (NF-κB) activation. Instead, activation of a different segment of the Imd pathway that branches off downstream of Tak1 and comprises activation of c-Jun N-terminal kinase (JNK) and forkhead transcription factor of the O subgroup (FoxO) signaling is necessary and sufficient to mediate the observed structural changes of the airways. Our findings imply that targeting JNK and FoxO signaling in the airways could be a promising strategy to interfere with disease-associated airway remodeling processes.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Drosophila Melanogaster, Asthma, Copd, Toll-like Receptor, Trachea, Tak1, Nf-kappab
ISSN (print) / ISBN 2211-1247
e-ISSN 2211-1247
Zeitschrift Cell Reports
Quellenangaben Band: 35, Heft: 1, Seiten: , Artikelnummer: 108956 Supplement: ,
Verlag Cell Press
Verlagsort 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute for Allergy Research (IAF)
Förderungen Priority Area Asthma & Allergy, Research Center Borstel
Leibniz Science Campus Evolung
Cluster of Excellence "PMI''
Cluster of Excellence "Inflammation@interfaces''
Deutsche Forschungsgemeinschaft (DFG), Germany