Allergic Triggers Associated With More Severe Asthma Exacerbations

CHEST Journal ◽  
2010 ◽  
Vol 138 (4) ◽  
pp. 310A ◽  
Author(s):  
Kathleen A. Sala ◽  
Alex M. Dressler ◽  
Taylor Aglio ◽  
Philip C. Spinella ◽  
Craig M. Schramm ◽  
...  
Keyword(s):  
Severe Asthma ◽  
Asthma Exacerbations

Meta-Analysis: Effect of Long-Acting β-Agonists on Severe Asthma Exacerbations and Asthma-Related Deaths

2006 ◽  
Vol 144 (12) ◽  
pp. 904 ◽  
Author(s):  
Shelley R. Salpeter ◽  
Nicholas S. Buckley ◽  
Thomas M. Ormiston ◽  
Edwin E. Salpeter
Keyword(s):  
Severe Asthma ◽  
Meta Analysis ◽  
Asthma Exacerbations ◽  
Long Acting

Childhood obesity increases duration of therapy during severe asthma exacerbations

2006 ◽  
Vol 7 (6) ◽  
pp. 617
Author(s):  
Christopher L. Carroll ◽  
Anita Bhandari ◽  
Aaron R. Zucker ◽  
Craig M. Schramm
Keyword(s):  
Childhood Obesity ◽  
Severe Asthma ◽  
Duration Of Therapy ◽  
Asthma Exacerbations

scholarly journals TLR3/TAK1 signalling regulates rhinovirus-induced interleukin-33 in bronchial smooth muscle cells

2020 ◽  
Vol 6 (4) ◽  
pp. 00147-2020
Author(s):  
Sangeetha Ramu ◽  
Jenny Calvén ◽  
Charalambos Michaeloudes ◽  
Mandy Menzel ◽  
Hamid Akbarshahi ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Severe Asthma ◽  
Poly I:C ◽  
Healthy Controls ◽  
Bronchial Smooth Muscle ◽  
Interleukin 33 ◽  
Asthma Exacerbations ◽  
Gene And Protein Expression ◽  
Bronchial Smooth Muscle Cells

BackgroundAsthma exacerbations are commonly associated with rhinovirus (RV) infection. Interleukin-33 (IL-33) plays an important role during exacerbation by enhancing Type 2 inflammation. Recently we showed that RV infects bronchial smooth muscle cells (BSMCs) triggering production of interferons and IL-33. Here we compared levels of RV-induced IL-33 in BSMCs from healthy and asthmatic subjects, and explored the involvement of pattern-recognition receptors (PRRs) and downstream signalling pathways in IL-33 expression.MethodBSMCs from healthy and severe and non-severe asthmatic patients were infected with RV1B or stimulated with the PRR agonists poly(I:C) (Toll-like receptor 3 (TLR3)), imiquimod (TLR7) and poly(I:C)/LyoVec (retinoic acid-inducible gene 1 (RIG-I)/melanoma differentiation-associated protein 5 (MDA5)). Knockdown of TLR3, RIG-I and MDA5 was performed, and inhibitors targeting TBK1, nuclear factor-κB (NF-κB) and transforming growth factor (TGF)-β-activated kinase 1 (TAK1) were used. Gene and protein expression were assessed.ResultsRV triggered IL-33 gene and protein expression in BSMCs. BSMCs from patients with non-severe asthma showed higher baseline and RV-induced IL-33 gene expression compared to cells from patients with severe asthma and healthy controls. Furthermore, RV-induced IL-33 expression in BSMCs from healthy and asthmatic individuals was attenuated by knockdown of TLR3. Inhibition of TAK1, but not NF-κB or TBK1, limited RV-induced IL-33. The cytokine secretion profile showed higher production of IL-33 in BSMCs from patients with non-severe asthma compared to healthy controls upon RV infection. In addition, BSMCs from patients with non-severe asthma had higher levels of RV-induced IL-8, TNF-α, IL-1β, IL-17A, IL-5 and IL-13.ConclusionRV infection caused higher levels of IL-33 and increased pro-inflammatory and Type 2 cytokine release in BSMCs from patients with non-severe asthma. RV-induced IL-33 expression was mainly regulated by TLR3 and downstream via TAK1. These signalling molecules represent potential therapeutic targets for treating asthma exacerbations.

scholarly journals Job strain and the risk of severe asthma exacerbations: a meta-analysis of individual-participant data from 100 000 European men and women

Allergy ◽  
2014 ◽  
Vol 69 (6) ◽  
pp. 775-783 ◽  
Author(s):  
K. Heikkilä ◽  
I. E. H. Madsen ◽  
S. T. Nyberg ◽  
E. I. Fransson ◽  
H. Westerlund ◽  
...  
Keyword(s):  
Severe Asthma ◽  
Job Strain ◽  
Meta Analysis ◽  
Individual Participant Data ◽  
Men And Women ◽  
Asthma Exacerbations ◽  
Individual Participant
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