Asthma and lower airway diseaseDetection of pathogenic bacteria during rhinovirus infection is associated with increased respiratory symptoms and asthma exacerbations
Section snippets
Study subjects and design
Children included in this analysis were enrolled in a larger study (RhinoGen) to determine genetic correlates with more severe rhinovirus-induced illnesses. Of the 383 children participating in RhinoGen, 308 children aged 4 to 12 years submitted samples during a peak rhinovirus season. Starting the first Saturday of September 2007, 2008, or 2009, nasal samples were collected weekly for a total of 5 consecutive weeks. Children, with the help of their parents, were instructed to record upper
Subjects' characteristics
Of the 383 children enrolled in RhinoGen, 54 had insufficient quantity of nasal samples to allow analysis for both viruses and bacteria, whereas an additional 19 subjects did not submit at least 4 (80%) of the 5 scheduled nasal samples, and 2 additional subjects did not complete at least 40 days (80%) of symptom diaries. Therefore a total of 308 (80%) subjects were included in the final analysis (see Fig E1 in this article's Online Repository at www.jacionline.org).
Of the 308 subjects enrolled,
Discussion
In this study we tested 2 hypotheses to determine the role of bacterial pathogens in rhinovirus-induced respiratory symptoms and exacerbations of asthma. First, we predicted that detection of bacterial pathogens would be increased in children with asthma compared with their nonasthmatic counterparts; however, this was not the case. We also hypothesized that common bacterial pathogens contribute to rhinovirus-induced illness severity, and thus these bacteria would be more prevalent during
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The following National Institutes of Health (NIH) grants supported this research: U19 AI070503-01 (RhinoGen); P01 HL070831 (Childhood Origins of Asthma); 1UL1RR025011 from the Clinical and Translational Science Award (CTSA) program of the National Center for Research Resources, NIH; and T32AI007635 (University of Wisconsin Allergy Research Training program).
Disclosure of potential conflict of interest: K. M. Kloepfer, T. E. Pappas, M. D. Evans, and Y. A. Bochkov have received research support from the National Institutes of Health (NIH). R. E. Gangnon has received research support from the National Heart, Lung, and Blood Institute (NHLBI). D. J. Jackson has received consulting fees from GlaxoSmithKline and Genentech. R. F. Lemanske, Jr, has been supported by a grant, consultancy fees, and participation fees from the NIH; is a board member for the American Academy of Allergy, Asthma & Immunology (AAAAI); has received consultancy fees from Merck, Sepracor, SA Boney and Associates, GlaxoSmithKline, the American Institute of Research, Genentech, Double Helix Development, and Boehringer Ingelheim; is employed by the University of Wisconsin School of Medicine and Public Health; has received research support from the NHLBI and Pharmaxis; has received lecture fees from the Michigan Public Health Institute, Allegheny General Hospital, the American Academy of Pediatrics, West Allegheny Health Systems, California Chapter 4, AAP, the Colorado Allergy Society, the Pennsylvania Allergy and Asthma Association, Harvard Pilgrim Health, the California Society of Allergy, the NYC Allergy Society, the World Allergy Organization, the American College of Chest Physicians, APAPARI, and the Western Society of Allergy, Asthma, and Immunology; has received payment for manuscript preparation from the AAAAI; and has received royalties from Elsevier and UpToDate. J. E. Gern has received research support from the NIH, Merck, AstraZeneca, and GlaxoSmithKline and has received personal fees from GlaxoSmithKline, Biota, Centocor, Boehringer Ingelheim, MedImmune, Theraclone, Merck, and Gilead. The rest of the authors declare that they have no relevant conflicts of interest.