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Determinants of sputum neutrophilia after experimental infection with rhinovirus (RV) 16
S268 Abstracts
J ALLERGY CLIN IMMUNOL FEBRUARY 2004
968
Determinants of Sputum Neutrophilia After Experimental Infection With Rhinovirus (RV) 16
TUESDAY
R. F. Vrtis, J. E. Gern, E. A. Hanzel, W. W. Busse; Medicine, University of Wisconsin, Madison, WI. RATIONALE: Although lower airway neutrophilia occurs during RV infections and may be an important component of the inflammatory response to cause an asthma exacerbation, the mechanisms of this infection-immune interaction are incompletely understood. METHODS: To define the relationship and kinetics of neutrophilic inflammation and viral load in the lower airway, 13 allergic asthma and 6 normal subjects were experimentally inoculated with RV16. During the infection, nasal lavage and sputum specimens were obtained serially to measure cellular inflammation and RV RNA by real time PCR. RESULTS: After inoculation, sputum RV RNA peaked at 3-7 days (range <0.5 to 4.6 X 105 PCR units), and sputum neutrophils were significantly increased at 7 days (6.5 vs 2.5 X 105 cells/gram at baseline, p<0.001). During the acute cold, a positive correlation was observed between the sputum viral load and the number of neutrophils (rs=0.73, p=0.01). At the recovery phase, sputum neutrophilia persisted in subjects still shedding virus from the nose (rs=0.72, p=0.02). CONCLUSIONS: Experimental infection with RV induces a variable degree of sputum neutrophilia, which appears to be dependent on viral replication in the lower airway, as well as prolonged viral shedding. These data suggest that greater viral replication in the lower airway, perhaps due to impaired antiviral responses, is a risk factor for bronchial inflammation and could contribute to respiratory infection induced asthma exacerbations. Funding: NIH Grant #5 P01 AI050500 & GCRC grant #MO1 RR03186
J ALLERGY CLIN IMMUNOL FEBRUARY 2004
968
Determinants of Sputum Neutrophilia After Experimental Infection With Rhinovirus (RV) 16
TUESDAY
R. F. Vrtis, J. E. Gern, E. A. Hanzel, W. W. Busse; Medicine, University of Wisconsin, Madison, WI. RATIONALE: Although lower airway neutrophilia occurs during RV infections and may be an important component of the inflammatory response to cause an asthma exacerbation, the mechanisms of this infection-immune interaction are incompletely understood. METHODS: To define the relationship and kinetics of neutrophilic inflammation and viral load in the lower airway, 13 allergic asthma and 6 normal subjects were experimentally inoculated with RV16. During the infection, nasal lavage and sputum specimens were obtained serially to measure cellular inflammation and RV RNA by real time PCR. RESULTS: After inoculation, sputum RV RNA peaked at 3-7 days (range <0.5 to 4.6 X 105 PCR units), and sputum neutrophils were significantly increased at 7 days (6.5 vs 2.5 X 105 cells/gram at baseline, p<0.001). During the acute cold, a positive correlation was observed between the sputum viral load and the number of neutrophils (rs=0.73, p=0.01). At the recovery phase, sputum neutrophilia persisted in subjects still shedding virus from the nose (rs=0.72, p=0.02). CONCLUSIONS: Experimental infection with RV induces a variable degree of sputum neutrophilia, which appears to be dependent on viral replication in the lower airway, as well as prolonged viral shedding. These data suggest that greater viral replication in the lower airway, perhaps due to impaired antiviral responses, is a risk factor for bronchial inflammation and could contribute to respiratory infection induced asthma exacerbations. Funding: NIH Grant #5 P01 AI050500 & GCRC grant #MO1 RR03186