Infantile Wheeze Research Articles

Eosinophil cationic protein and interleukin‐8 levels in bronchial lavage fluid from children with asthma and infantile wheeze

It has been shown previously that airway eosinophils characterize childhood asthma and neutrophils contribute to the pathophysiology of both infantile wheezing and asthma. Therefore, eosinophil cationic protein (ECP) and interleukin-8 (IL-8) levels in bronchoalveolar lavage fluid (BALF) from asthmatics (n = 16) and infantile wheezers (n = 30) were analyzed as markers of eosinophil- and neutrophil-mediated inflammation. To aid the interpretation, a control group of children (n = 10) with no lower airway pathology were included. Disease severity was assessed by using a symptom score. Surprisingly, no significant difference was found in IL-8 or ECP levels among asthma, infantile wheeze, and control groups. Asthma was characterized by: a correlation between ECP levels and eosinophil counts (r = 0.618, p = 0.014); a correlation between neutrophil number and IL-8 levels (r = 0.747, p = 0.002); and increasing IL-8 levels with symptom score (p = 0.03). In infantile wheezers, IL-8 levels were poorly related to neutrophil number but were significantly increased when neutrophils were > 10%. Although detectable levels were found in all but one symptomatic infant, IL-8 concentrations did not reflect the symptom score in infantile wheeze. ECP was unexpectedly correlated to neutrophil percentages (Rho = 0.832, p = 0.001), and a threshold of ECP>20 ng/ml was associated with persistent symptoms in these infantile wheezers. Hence, in accordance with BALF cellularity, activation of eosinophils was suggested by raised levels of ECP in childhood asthma, but not in infantile wheeze. Neutrophil-mediated inflammation appeared to better reflect the severity of asthma than that of infantile wheeze. Although its meaning remains to be elucidated, ECP was suggested to be a helpful indicator of persistent infantile wheeze. However, its utility as a marker predicting ongoing asthma remains to be established.

Soluble intercellular adhesion molecule-1 (sICAM-1) and interferon-gamma in bronchoalveolar lavage fluid from children with airway diseases.

We have previously described that in bronchoalveolar lavage fluid (BALF), eosinophils characterize asthma and neutrophils are more prominent in infantile wheeze. In this study, we hypothesized that intercellular adhesion molecule 1 (ICAM-1) and interferon-gamma (IFN-gamma) would have a role in promoting migration of both cell types into the airway. To investigate this, we measured soluble (s) ICAM-1 in 68 BALFs from infants and young children with various respiratory problems. Children with asthma were characterized by significantly raised sICAM compared with those with chronic cough without wheeze (p = 0.05) or control subjects with no lower airway pathology (p = 0.045). The levels correlated with disease severity (evaluated with a symptom score) and with lymphocyte numbers. IFN-gamma levels were also raised in children with asthma compared with those with chronic cough (p = 0.05), but there was no correlation with disease activity. Infantile wheeze was characterized by a linear correlation between sICAM-1 and IFN-gamma (r = 0.55; p = 0.002). sICAM-1 levels in infantile wheeze correlated with the severity of the disease and lymphocyte numbers. IFN-gamma levels were elevated in the wheezers treated with inhaled steroids compared with untreated infants (p = 0.03). Although sICAM-1 levels were increased in those with severe cough, no characteristic inflammatory profile was found in the group with chronic cough. Our study suggests that ICAM-1 and IFN-gamma play a role in the activity of the inflammatory process in asthma in childhood and possibly in some infant wheezers, in whom IFN-gamma may be one of the factors increasing the expression of ICAM-1. The role of IFN-gamma, a T helper-1 cytokine, in children with asthma remains to be fully understood.

Bronchoalveolar cell profiles in children with asthma, infantile wheeze, chronic cough, or cystic fibrosis.

Differential cell counts of bronchoalveolar lavage (BAL) have been reported in normal children but few data on cellular profiles in bronchial diseases in childhood are available. We determined the BAL cell profiles of 72 children divided into 5 groups: asthma (n = 14), chronic cough (n = 12), infantile wheeze (n = 26), cystic fibrosis (n = 10), and control (n = 10). The highest total cell, eosinophil, and neutrophil counts were found in children with cystic fibrosis. The cell profile of children with chronic cough was similar to that of control children. Asthma and infantile wheeze were characterized by a high median ratio of eosinophils (3%) and neutrophils (12%), respectively. In both diseases, epithelial shedding was suggested by an elevated epithelial cell count, 13.5 and 12%, respectively. Lymphocyte subset analysis showed a higher proportion of CD8 cells (58 versus 40%) and therefore a lower CD4/CD8 ratio (0.266 versus 0. 455) in children with asthma compared with infantile wheezers (p = 0. 02). Irrespective of the presence or absence of radiological abnormalities, a proportion of neutrophils > 10%, was found in one-third of the children with asthma and in half of the infantile wheezers, and was related to symptom severity. We suggest that neutrophil-mediated inflammation, with or without bacterial infection, may contribute to symptoms of asthma in childhood. Chronic cough, however, is not associated with the cell profiles suggestive of asthma and in isolation should not be treated with prophylactic antiasthma drugs.

The prevalence of and risk factors for atopy in early childhood: A whole population birth cohort study

Objectives: A birth cohort was followed-up to age 4 years to record the development of allergic disorders and to study the influence of genetic and environmental factors. Methods: Information on family history and environmental factors was obtained at birth, and serum cord IgE was measured. At age 4 years, 1218 children were reviewed. Results: By age 4 years, 27% of the children had symptoms of allergic disease. Period prevalence of asthma increased from 8.7% in infancy to 14.9% at 4 years. Family history of atopy was the single most important risk factor for atopy in children. Sibling atopy was a stronger predictor of clinical disease than maternal or paternal atopy, whereas paternal atopy, male sex, and high cord IgE were significant for the development of allergen sensitization. Children of asthmatic mothers were three times more likely to have asthma (odds ratio [OR]: 3.0, 95% confidence interval [CI]: 1.6-5.8) and rhinitis (OR: 2.9, CI: 1.1-7.4). Formula feeding before 3 months of age predisposed to asthma at age 4 years (OR: 1.8, CI: 1.2-2.6). The effect of maternal smoking on childhood wheeze seen at 1 and 2 years was lost by age 4, except for a subgroup with negative skin test responses (nonatopic asthma). Less than half (46%) of the infantile wheezers were still wheezing at 4 years of age. Conclusion: Family history of atopy remains the most important risk factor for atopy in children, but other markers can be identified with a potential for intervention at an early age.

238 IL-8 and soluble ICAM-1 (sICAM-1) concentration in bronchoalveolar lavage (BAL) of asthmatic children and infantile wheezers

238 IL-8 and soluble ICAM-1 (sICAM-1) concentration in bronchoalveolar lavage (BAL) of asthmatic children and infantile wheezers

509 Bronchoalveolar lavage (BAL) cellularity in asthmatic children and infantile wheezers: Role of neutrophils

509 Bronchoalveolar lavage (BAL) cellularity in asthmatic children and infantile wheezers: Role of neutrophils