IL-1/inhibitory kappaB kinase epsilon-induced glycolysis augment epithelial effector function and promote allergic airways disease.

Qian, Xi; Aboushousha, Reem; van de Wetering, Cheryl; Chia, Shi B.; Amiel, Eyal; Schneider, Robert W.; van der Velden, Jos L. J.; Lahue, Karolyn G.; Hoagland, Daisy A.; Casey, Dylan T.; Daphtary, Nirav; Ather, Jennifer L.; Randall, Matthew J.; Aliyeva, Minara; Black, Kendall E.; Chapman, David G.; Lundblad, Lennart K. A.; McMillan, David H.; Dixon, Anne E.; Anathy, Vikas; Irvin, Charles G.; Poynter, Matthew E.; Wouters, Emiel F. M.; Vacek, Pamela M.; HENKET, Monique; SCHLEICH, FLorence; Louis, Renaud; van der Vliet, Albert; Janssen-Heininger, Yvonne M. W.

doi:10.1016/j.jaci.2017.08.043

Article (Scientific journals)

IL-1/inhibitory kappaB kinase epsilon-induced glycolysis augment epithelial effector function and promote allergic airways disease.

Qian, Xi; Aboushousha, Reem; van de Wetering, Cheryl et al.

2017 • In Journal of Allergy and Clinical Immunology

Peer Reviewed verified by ORBi

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https://hdl.handle.net/2268/240203

DOI
10.1016/j.jaci.2017.08.043

PubMed
29108965

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Keywords :

Asthma; IL-1; glycolysis; house dust mite; inhibitor of kappaB kinase epsilon; lactate; lactate dehydrogenase A

Abstract :

[en] BACKGROUND: Emerging studies suggest that enhanced glycolysis accompanies inflammatory responses. Virtually nothing is known about the relevance of glycolysis in patients with allergic asthma. OBJECTIVES: We sought to determine whether glycolysis is altered in patients with allergic asthma and to address its importance in the pathogenesis of allergic asthma. METHODS: We examined alterations in glycolysis in sputum samples from asthmatic patients and primary human nasal cells and used murine models of allergic asthma, as well as primary mouse tracheal epithelial cells, to evaluate the relevance of glycolysis. RESULTS: In a murine model of allergic asthma, glycolysis was induced in the lungs in an IL-1-dependent manner. Furthermore, administration of IL-1beta into the airways stimulated lactate production and expression of glycolytic enzymes, with notable expression of lactate dehydrogenase A occurring in the airway epithelium. Indeed, exposure of mouse tracheal epithelial cells to IL-1beta or IL-1alpha resulted in increased glycolytic flux, glucose use, expression of glycolysis genes, and lactate production. Enhanced glycolysis was required for IL-1beta- or IL-1alpha-mediated proinflammatory responses and the stimulatory effects of IL-1beta on house dust mite (HDM)-induced release of thymic stromal lymphopoietin and GM-CSF from tracheal epithelial cells. Inhibitor of kappaB kinase epsilon was downstream of HDM or IL-1beta and required for HDM-induced glycolysis and pathogenesis of allergic airways disease. Small interfering RNA ablation of lactate dehydrogenase A attenuated HDM-induced increases in lactate levels and attenuated HDM-induced disease. Primary nasal epithelial cells from asthmatic patients intrinsically produced more lactate compared with cells from healthy subjects. Lactate content was significantly higher in sputum supernatants from asthmatic patients, notably those with greater than 61% neutrophils. A positive correlation was observed between sputum lactate and IL-1beta levels, and lactate content correlated negatively with lung function. CONCLUSIONS: Collectively, these findings demonstrate that IL-1beta/inhibitory kappaB kinase epsilon signaling plays an important role in HDM-induced glycolysis and pathogenesis of allergic airways disease.

Disciplines :

Cardiovascular & respiratory systems

Author, co-author :

Qian, Xi

Aboushousha, Reem

van de Wetering, Cheryl

Chia, Shi B.

Amiel, Eyal

Schneider, Robert W.

van der Velden, Jos L. J.

Lahue, Karolyn G.

Hoagland, Daisy A.

Casey, Dylan T.

More authors (19 more)

Language :

English

Title :

IL-1/inhibitory kappaB kinase epsilon-induced glycolysis augment epithelial effector function and promote allergic airways disease.

Publication date :

November 2017

Journal title :

Journal of Allergy and Clinical Immunology

ISSN :

0091-6749

eISSN :

1097-6825

Publisher :

Mosby, United States - Missouri

Peer reviewed :

Peer Reviewed verified by ORBi

Additional URL :

https://www.sciencedirect.com/science/article/pii/S0091674917316639?via%3Dihub

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Available on ORBi :

since 12 October 2019

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