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Interleukin-10 gene expression in acute virus-induced asthma #MMPMID15894599
Am J Respir Crit Care Med 2005[Aug]; 172 (4): 433-9 PMID15894599show ga
RATIONALE: Virus-induced asthma is characterized by marked neutrophil influx and eosinophil degranulation, suggesting a mode of immunopathogenesis different from that of allergen-induced asthma. OBJECTIVES: This study compared induced sputum cytokine responses in subjects with severe asthma exacerbation and respiratory virus infection with those of patients with stable asthma, healthy control subjects, and virus-infected nonasthmatic subjects. METHODS: Subject infection status and pulmonary history were established on the basis of common cold and asthma questionnaires, and lung function and atopy tests were performed. Respiratory virus infection was diagnosed by cell culture and direct polymerase chain reaction, using induced sputum. The induced sputum cellular profile was examined and cytokine gene expression was assessed by quantitative real-time polymerase chain reaction. RESULTS: A respiratory virus was detected in 78% of subjects with acute asthma. Specific viruses detected were rhinovirus (83%), influenza (15%), enterovirus (4%), and respiratory syncytial virus (2%). Virus-infected subjects with acute asthma or no asthma had increased RANTES (regulated on activation, normal T cell expressed and secreted) and macrophage inflammatory protein-1alpha messenger RNAs compared with other groups. Interleukin (IL)-10 mRNA was significantly increased in virus-infected acute asthma and reduced on recovery from acute asthma. IL-5, eotaxin, and IL-8 mRNA transcripts were similar across groups. CONCLUSIONS: Asthma exacerbation triggered by respiratory virus infection is characterized by increased IL-10 gene expression that may explain the suppressed eosinophil influx in acute asthma. Airway neutrophilia due to respiratory virus infection is associated with chemokine gene expression involving RANTES and macrophage inflammatory protein-1alpha.
Am+J+Respir+Crit+Care+Med 2005 ; 172 (4): 433-9
