RATIONALE: Epidemiologic studies have shown that, in atopic children, wheezing is more likely to persist into adulthood, eventually becoming asthma, whereas it appears to resolve by adolescence in nonatopic children. OBJECTIVES: To investigate whether among children with multitrigger wheeze responsive to bronchodilators the airway pathology would be different in nonatopic wheezers, who are often considered nonasthmatic, compared with atopic wheezers, who are more frequently diagnosed as having asthma. METHODS: Bronchial biopsies were obtained from 55 children undergoing bronchoscopy for appropriate clinical indications: 18 nonatopic children with multitrigger wheeze (median age, 5 yr; range, 2-10 yr), 20 atopic children with multitrigger wheeze (medan age, 5 yr; range, 2-15 yr), and 17 control children with no atopy or wheeze (median age, 4; range, 2-14 yr). By histochemistry and immunohistochemistry, we quantified epithelial loss, basement membrane thickness, angiogenesis, inflammatory cells, IL-4(+,) and IL-5(+) cells in subepithelium. MEASUREMENTS AND MAIN RESULTS: Unexpectedly, all pathologic features examined were similar in atopic and nonatopic wheezing children. Compared with control subjects, both nonatopic and atopic wheezing children had increased epithelial loss (P = 0.03 and P = 0.002, respectively), thickened basement membrane (both P < 0.0001), and increased number of vessels (P = 0.003 and P = 0.03, respectively) and eosinophils (P < 0.0001 and P = 0.002, respectively). Moreover, they had increased cytokine expression, which was highly significant for IL-4 (P = 0.002 and P = 0.0001, respectively) and marginal for IL-5 (P = 0.02 and P = 0.08, respectively). CONCLUSIONS: This study shows that the airway pathology typical of asthma is present in nonatopic wheezing children just as in atopic wheezing children. These results suggest that, when multitrigger wheezing responsive to bronchodilators is present, it is associated with pathologic features of asthma even in nonatopic children.
RATIONALE: Epidemiologic studies have shown that, in atopic children, wheezing is more likely to persist into adulthood, eventually becoming asthma, whereas it appears to resolve by adolescence in nonatopic children. OBJECTIVES: To investigate whether among children with multitrigger wheeze responsive to bronchodilators the airway pathology would be different in nonatopic wheezers, who are often considered nonasthmatic, compared with atopic wheezers, who are more frequently diagnosed as having asthma. METHODS: Bronchial biopsies were obtained from 55 children undergoing bronchoscopy for appropriate clinical indications: 18 nonatopic children with multitrigger wheeze (median age, 5 yr; range, 2-10 yr), 20 atopic children with multitrigger wheeze (medan age, 5 yr; range, 2-15 yr), and 17 control children with no atopy or wheeze (median age, 4; range, 2-14 yr). By histochemistry and immunohistochemistry, we quantified epithelial loss, basement membrane thickness, angiogenesis, inflammatory cells, IL-4(+,) and IL-5(+) cells in subepithelium. MEASUREMENTS AND MAIN RESULTS: Unexpectedly, all pathologic features examined were similar in atopic and nonatopic wheezing children. Compared with control subjects, both nonatopic and atopic wheezingchildren had increased epithelial loss (P = 0.03 and P = 0.002, respectively), thickened basement membrane (both P < 0.0001), and increased number of vessels (P = 0.003 and P = 0.03, respectively) and eosinophils (P < 0.0001 and P = 0.002, respectively). Moreover, they had increased cytokine expression, which was highly significant for IL-4 (P = 0.002 and P = 0.0001, respectively) and marginal for IL-5 (P = 0.02 and P = 0.08, respectively). CONCLUSIONS: This study shows that the airway pathology typical of asthma is present in nonatopic wheezing children just as in atopic wheezingchildren. These results suggest that, when multitrigger wheezing responsive to bronchodilators is present, it is associated with pathologic features of asthma even in nonatopic children.
Authors: Rodney D Britt; Arij Faksh; Elizabeth Vogel; Richard J Martin; Christina M Pabelick; Y S Prakash Journal: Expert Rev Respir Med Date: 2013-10-03 Impact factor: 3.772
Authors: Stephen T Holgate; Hasan S Arshad; Graham C Roberts; Peter H Howarth; Philipp Thurner; Donna E Davies Journal: Clin Sci (Lond) Date: 2009-12-23 Impact factor: 6.124
Authors: Steve Abman; Alan Jobe; Victor Chernick; Carol Blaisdell; Mario Castro; Maria I Ramirez; James E Gern; Garry Cutting; Greg Redding; James S Hagood; Jeffrey Whitsett; Steve Abman; J Usha Raj; Robyn Barst; Gregory J Kato; David Gozal; Gabriel G Haddad; Nanduri R Prabhakar; Estelle Gauda; Fernando D Martinez; Robert Tepper; Robert E Wood; Frank Accurso; W Gerald Teague; Jose Venegas; F Sessions Cole; Rosalind J Wright; Dorothy Gail; Aaron Hamvas; Carolyn Kercsmar; James Kiley; Gail Weinmann Journal: Pediatr Pulmonol Date: 2009-01
Authors: Mario Castro; Maria I Ramirez; James E Gern; Garry Cutting; Greg Redding; James S Hagood; Jeffrey Whitsett; Steve Abman; J Usha Raj; Robyn Barst; Gregory J Kato; David Gozal; Gabriel G Haddad; Nanduri R Prabhakar; Estelle Gauda; Fernando D Martinez; Robert Tepper; Robert E Wood; Frank Accurso; W Gerald Teague; Jose Venegas; F Sessions Cole; Rosalind J Wright Journal: Proc Am Thorac Soc Date: 2009-01-15