Altered eosinophil levels as a result of viral infection in asthma exacerbation in childhood

Respiratory viral infection is known to be a significant cause of asthma exacerbation. Eosinophils have been considered to play an important role in the pathogenesis of virus‐induced asthma exacerbations. To determine how often asthma exacerbation is caused by virus infections and to examine the relationship between eosinophilia and asthma episode, we investigated 64 children who experienced asthma attacks between October 1999 and March 2000. We used rapid enzyme immunoassays to detect antigens of respiratory syncytial virus (RSV), influenza A virus, and adenovirus in nasopharyngeal secretions (NPS) of these children, and enumerated eosinophils in the blood and NPS. We detected RSV in 27% and influenza A virus in 17% of the patients. No adenovirus infection or RSV/influenza A co‐infection was detected. RSV‐infected children were younger (3.85 ± 0.83 years old) than influenza A virus‐infected patients (5.23 ± 1.34 years old). Eighty‐two per cent of patients in the RSV group and 36% of patients in the influenza A virus group had moderate‐to‐severe asthma episodes (p < 0.05). In RSV‐infected children, the eosinophil counts in NPS were higher in the ‘severe’ group, and younger patients had a greater number of eosinophils in their NPS than older patients (p < 0.05). These trends were not found in influenza A virus patients. In conclusion, our results indicate that, compared with influenza A virus‐induced asthma attacks, RSV infection had a higher probability of being associated with asthma exacerbation in infants and younger children and induced attacks of greater severity. The increase in the number of eosinophils in the NPS of RSV‐infected children may be responsible, in part, for these differences.

[1]  D. Sherrill,et al.  Respiratory syncytial virus in early life and risk of wheeze and allergy by age 13 years , 1999, The Lancet.

[2]  T. Okubo,et al.  Influenza A virus infection increases IgE production and airway responsiveness in aerosolized antigen-exposed mice , 1998, Journal of Allergy and Clinical Immunology.

[3]  E. Gelfand,et al.  Respiratory syncytial virus infection results in airway hyperresponsiveness and enhanced airway sensitization to allergen. , 1997, The Journal of clinical investigation.

[4]  F. Hargreave,et al.  Measuring airway inflammation in asthma: eosinophils and eosinophilic cationic protein in induced sputum compared with peripheral blood. , 1997, The Journal of allergy and clinical immunology.

[5]  A. Milner,et al.  Respiratory status and allergy nine to 10 years after acute bronchiolitis , 1997, Archives of disease in childhood.

[6]  R. Neville,et al.  Role of viral infections in exacerbations of asthma , 1995, BMJ.

[7]  Stephen T Holgate,et al.  Community study of role of viral infections in exacerbations of asthma in 9-11 year old children , 1995, BMJ.

[8]  B. Björkstén,et al.  Asthma and immunoglobulin E antibodies after respiratory syncytial virus bronchiolitis: a prospective cohort study with matched controls. , 1995, Pediatrics.

[9]  S. Johnston,et al.  Lower airways inflammation during rhinovirus colds in normal and in asthmatic subjects. , 1995, American journal of respiratory and critical care medicine.

[10]  F. Hayden,et al.  Risk factors for acute wheezing in infants and children: viruses, passive smoke, and IgE antibodies to inhalant allergens. , 1993, Pediatrics.

[11]  M. Saijo,et al.  Respiratory syncytial virus infection in lower respiratory tract and asthma attack in hospitalized children in North Hokkaido, Japan , 1993, Acta paediatrica Japonica : Overseas edition.

[12]  S. Johnston,et al.  Viruses as precipitants of asthma symptoms. I. Epidemiology , 1992, Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology.

[13]  N. Flavahan,et al.  The eosinophil as a mediator of damage to respiratory epithelium: a model for bronchial hyperreactivity. , 1988, The Journal of allergy and clinical immunology.

[14]  Josephine Antonette Curcio Publication No. _______ , 2003 .