• Publications
  • Influence
T-helper type 2-driven inflammation defines major subphenotypes of asthma.
Asthma can be divided into at least two distinct molecular phenotypes defined by degree of Th2 inflammation, and Th2 cytokines are likely to be a relevant therapeutic target in only a subset of patients with asthma. Expand
Genome-wide profiling identifies epithelial cell genes associated with asthma and with treatment response to corticosteroids
The findings show that airway epithelial cells in asthma have a distinct activation profile and identify direct and cell-autonomous effects of corticosteroid treatment on airway endothelial cells that relate to treatment responses and can now be the focus of specific mechanistic studies. Expand
Type 2 inflammation in asthma — present in most, absent in many
  • J. Fahy
  • Biology, Medicine
  • Nature Reviews Immunology
  • 2014
How dichotomizing asthma according to levels of type 2 inflammation — into 'T helper 2 (TH2)-high' and 'TH2-low' subtypes (endotypes) — has shaped the thinking about the pathobiology of asthma and has generated new interest in understanding the mechanisms of disease that are independent of type 1 inflammation is considered. Expand
Calcium-activated chloride channel TMEM16A modulates mucin secretion and airway smooth muscle contraction
It is shown that the recently identified calcium-activated chloride channel (CaCC) TMEM16A is expressed in the adult airway surface epithelium and ASM and significantly reduces mouse and human ASM contraction in response to cholinergic agonists. Expand
Tiotropium bromide step-up therapy for adults with uncontrolled asthma.
When added to an inhaled glucocorticoid, tiotropium improved symptoms and lung function in patients with inadequately controlled asthma and its effects appeared to be equivalent to those with the addition of salmeterol. Expand
Hyperplasia of smooth muscle in mild to moderate asthma without changes in cell size or gene expression.
It is concluded that airway smooth muscle proliferation is a pathologic characteristic of subjects with mild to moderate asthma, however, smooth muscle cells in mild tomoderate asthma do not show hypertrophy or gene expression changes of a hypercontractile phenotype observed in vitro. Expand
Asthma outcomes: biomarkers.
The working group participants propose the use of multiallergen screening in all asthma clinical trials to characterize study populations with respect to atopic status and develop standard procedures to harmonize sample collection for clinical trial biorepositories. Expand
Effects of treatment with anti-immunoglobulin E antibody omalizumab on airway inflammation in allergic asthma.
The lack of effect of omalizumab on methacholine responsiveness suggests that IgE or eosinophils may not be causally linked to airway hyperresponsiveness to Methacholine in mild to moderate asthma. Expand
Prominent neutrophilic inflammation in sputum from subjects with asthma exacerbation.
Neutrophils predominate more frequently than eosinophils as the major inflammatory cell in sputum from patients with asthma in acute exacerbation, which suggests that IL-8 may mediate airway neutrophilia in acute asthma and that neutrophil elastase may mediated mucin glycoprotein hypersecretion in acute allergy. Expand
Mild and moderate asthma is associated with airway goblet cell hyperplasia and abnormalities in mucin gene expression.
It is concluded that even mild asthma is associated with goblet cell hyperplasia and increased stored mucin in the airway epithelium, whereas moderate asthma isassociated with increased stored bronchial mucin and secreted mucin. Expand