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Status: Bibliographieeintrag

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Verfasst von:Anagnostopoulou, Pinelopi [VerfasserIn]   i
 Dürr, Julia [VerfasserIn]   i
 Agrawal, Raman [VerfasserIn]   i
 Schatterny, Jolanthe [VerfasserIn]   i
 Mall, Marcus A. [VerfasserIn]   i
Titel:SLC26A9-mediated chloride secretion prevents mucus obstruction in airway inflammation
Verf.angabe:Pinelopi Anagnostopoulou, Brigitte Riederer, Julia Duerr, Sven Michel, Aristea Binia, Raman Agrawal, Xuemei Liu, Katrin Kalitzki, Fang Xiao, Mingmin Chen, Jolanthe Schatterny, Dorothee Hartmann, Thomas Thum, Michael Kabesch, Manoocher Soleimani, Ursula Seidler, and Marcus A. Mall
E-Jahr:2012
Jahr:September 4, 2012
Umfang:6 S.
Fussnoten:Gesehen am 25.05.2018
Titel Quelle:Enthalten in: The journal of clinical investigation
Ort Quelle:Ann Arbor, Mich. : ASCJ, 1924
Jahr Quelle:2012
Band/Heft Quelle:122(2012), 10, Seite 3629-3634
ISSN Quelle:1558-8238
Abstract:Asthma is a chronic condition with unknown pathogenesis, and recent evidence suggests that enhanced airway epithelial chloride (Cl-) secretion plays a role in the disease. However, the molecular mechanism underlying Cl- secretion and its relevance in asthma pathophysiology remain unknown. To determine the role of the solute carrier family 26, member 9 (SLC26A9) Cl- channel in asthma, we induced Th2-mediated inflammation via IL-13 treatment in wild-type and Slc26a9-deficient mice and compared the effects on airway ion transport, morphology, and mucus content. We found that IL-13 treatment increased Cl- secretion in the airways of wild-type but not Slc26a9-deficient mice. While IL-13-induced mucus overproduction was similar in both strains, treated Slc26a9-deficient mice exhibited airway mucus obstruction, which did not occur in wild-type controls. In a study involving healthy children and asthmatics, a polymorphism in the 3' UTR of SLC26A9 that reduced protein expression in vitro was associated with asthma. Our data demonstrate that the SLC26A9 Cl- channel is activated in airway inflammation and suggest that SLC26A9-mediated Cl- secretion is essential for preventing airway obstruction in allergic airway disease. These results indicate that SLC26A9 may serve as a therapeutic target for airway diseases associated with mucus plugging.
DOI:doi:10.1172/JCI60429
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Kostenfrei: Volltext: http://dx.doi.org/10.1172/JCI60429
 : : https://doi.org/10.1172/JCI60429
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:3' Untranslated Regions
 Airway Obstruction
 Animals
 Antiporters
 Asthma
 Bronchitis
 Child
 Chlorides
 Cyclic AMP
 Cystic Fibrosis Transmembrane Conductance Regulator
 Epithelial Cells
 Genetic Predisposition to Disease
 Humans
 Interleukin-13
 Ion Transport
 Lung
 Mice
 Mucus
 Th2 Cells
 Tracheitis
K10plus-PPN:1575501996
Verknüpfungen:→ Zeitschrift

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