Patients with severe asthma showed higher epithelial expression of eotaxin-2. Levels of eotaxin-2 positively correlated with age of asthma onset, sputum eosinophils, and number of exacerbations and negatively correlated with FEV1 % predicted. Among patients with late-onset (but not early-onset) asthma, eotaxin-levels were higher in those with severe asthma. Sputum eosinophilia was more common among patients with late-onset asthma.
Lower L-arginine/ADMA ratio and negative correlation to BMI in late- versus early-onset asthma; may partly explain the inverse relationship between FeNO and BMI. Reduced L-arginine/ADMA ratio associated with reduced IgE and lung volumes, increased respiratory symptoms, and worse quality of life in late- but not early-onset asthma.
Leptin in visceral fat associated with AHR but not airway inflammation. Adipokine receptor was expressed in airway epithelium suggesting direct effects of adipokines on the airways.
Sideleva et al. 2012  Leivo-Korpela et al. 2011 
Nonobese women with newly-onset adult asthma
Leptin correlated positively with asthma symptom score and negatively with lung function even though no difference was found on adipokine levels between patients with asthma and healthy subjects. High baseline resistin predicted steeper decrease in serum ECP, EPX, and MPO during glucocorticoid treatment.
Late- and early-onset groups compared
Levels of YKL-40 were higher in asthma with poor control and exacerbations and atopy. When phenotypes were compared, highest levels of YKL-40 in obesity-related asthma and early-onset atopic asthma. Lower levels in nonatopic late-onset asthma.
Patients with moderate and severe asthma compared, approx. 85% with asthma onset 12 years in both groups
Levels of IFN- and IL-8 increased but IL-4 decreased in airway subepithelium of patients with severe poorly controlled asthma when compared to moderate disease. Patients with severe asthma had also increased number of eosinophils and neutrophils in sputum.
Patients with nonatopic adult-onset asthma and seropositivity to Chlamydia pneumoniae (IgG, IgA) had 4-fold-steeper decline in FEV1/FVC and accelerated decline in FEV1. C. pneumoniae infection might promote persistent airflow limitation in these patients.
Healthy controls, severe and nonsevere asthmatics compared
SA-IgE found more often in patients with severe asthma when compared to healthy subjects. Age of asthma onset highest in SA-IgE-positive group. SA-IgE associated with increased risk for asthma, severe asthma, hospitalizations, use of oral steroids, and lower FEV1.
Community-based population with adult-onset asthma
Risk factors for presence of SA-IgE were current smoking, older age, male sex, and inhalant allergen sensitization. SA-IgE was associated with current adult-onset asthma. Correlation between SA-IgE and total IgE.
Patients with newly diagnosed asthma (age range 16–98 years)
Smoking attenuated the age-related decrease in total IgE, blood eosinophils, and FeNO and maintained eosinophilic inflammation. Sputum TSLP levels were associated with sputum eosinophil % and pack-years. Current and ex-smokers had higher TSLP versus never-smokers. TSLP may be involved in elevating sputum eosinophils in smokers.
NR = not reported. ADMA = asymmetric dimethyl arginine, AHR = airway hyperresponsiveness, ECP = eosinophilic cationic protein, EPX = eosinophil peroxidase, MPO = myeloperoxidase, IFN = interferon, IL = interleukin, SA-IgE = Staphylococcus Aureus enterotoxin-specific immunoglobulin E, FEV1 = forced expiratory volume in 1 second, and TSLP = thymic stromal lymphopoietin.
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