Publications by authors named "L C Denlinger"
Rationale: Corticosteroid-responsive type 2 (T2) inflammation underlies the T2-high asthma endotype. However, we hypothesized that type 1 (T1) inflammation, possibly related to viral infection, may also influence corticosteroid response.
Objectives: To determine the frequency and within-patient variability of T1-high, T2-high, and T1/T2-high asthma endotypes and whether virally influenced T1-high disease influences corticosteroid response in asthma.
Background: Current asthma guidelines, including those of the European Respiratory Society (ERS) and American Thoracic Society (ATS), suboptimally predict asthma remission, disease severity, and health-care utilisation. We aimed to establish a novel approach to assess asthma severity based on asthma health-care burden data.
Methods: We analysed prospectively collected data from the Severe Asthma Research Program III (SARP III; USA) and the European Unbiased Biomarkers for the Prediction of Respiratory Disease Outcomes (U-BIOPRED; 11 European countries) to calculate a composite burden score based on asthma exacerbations and health-care utilisation, which was modified to include the use of short-acting beta agonists (SABAs) to reflect asthma symptom burden.
Mitochondrial DNA copy number variation in asthma risk, severity, and exacerbations.
J Allergy Clin Immunol
September 2024
Article Synopsis
- Asthma is linked to mitochondrial dysfunction, indicated by lower levels of mitochondrial DNA copy number (mtDNA-CN), which may serve as a proxy for mitochondrial health.* -
- A study using data from the UK Biobank and the Severe Asthma Research Program found that individuals with asthma consistently have lower mtDNA-CN levels compared to those without asthma, across all age groups.* -
- The research suggests that lower mtDNA-CN is associated with an increased risk of asthma exacerbations and is influenced by genetic factors rather than inflammation.*