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Respiratory syncytial virus-induced airway hyperresponsiveness is independent of IL-13 compared with that induced by allergen

Authors
 Jung Won Park  ;  Christian Taube  ;  Erwin W. Gelfand  ;  Debra D. Donaldson  ;  Azzeddine Dakhama  ;  Nobuaki Miyahara  ;  Katsuyuki Takeda  ;  Annette Balhorn  ;  Anthony Joetham  ;  Eun Seok Yang 
Citation
 JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol.112(6) : 1078-1087, 2003 
Journal Title
 JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY 
ISSN
 0091-6749 
Issue Date
2003
MeSH
Respiratory syncytial virus ; airway hyperresponsiveness ; IL-13
Keywords
Respiratory syncytial virus ; airway hyperresponsiveness ; IL-13
Abstract
BACKGROUND: IL-13 is a central mediator of allergen-induced airway hyperresponsiveness (AHR), but its role in respiratory syncytial virus (RSV)-induced AHR is not defined. The combination of allergen exposure and RSV infection is known to increase AHR and lung inflammation, but whether IL-13 regulates this increase is similarly not known. OBJECTIVE: Our objective was to determine the role of RSV infection and IL-13 on airway responsiveness and lung inflammation on sensitized and challenged mice. METHODS: Using a murine model of RSV infection and allergen exposure, we examined the role of IL-13 in the development of AHR and lung inflammation in IL-13 knockout mice, as well as using a potent IL-13 inhibitor (IL-13i). Mice were sensitized and challenged to allergen, and 6 days after the last challenge, they were infected with RSV. IL-13 was inhibited using an IL-13 receptor alpha(2)-human IgG fusion protein. AHR to inhaled methacholine was measured 6 days after infection, as was bronchoalveolar lavage fluid and lung inflammatory and cytokine responses. RESULTS: RSV-induced AHR was unaffected by the IL-13i, despite prevention of goblet cell hyperplasia. Similar results were seen in IL-13-deficient mice. In sensitized and challenged mice, RSV infection significantly increased AHR, and after IL-13i treatment, AHR was significantly reduced, but to the levels seen in RSV-infected mice alone. CONCLUSIONS: These results indicate that despite some similarities, the mechanisms leading to AHR induced by RSV are different from those that follow allergen sensitization and challenge. Because IL-13 inhibition is effective in preventing the increases in AHR and mucus production in sensitized and challenged mice infected with RSV, IL-13i could play an important role in preventing the consequences of viral infection in patients with allergic asthma.
Full Text
http://www.sciencedirect.com/science/article/pii/S0091674903022097
DOI
10.1016/j.jaci.2003.08.046
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Park, Jung Won(박중원) ORCID logo https://orcid.org/0000-0003-0249-8749
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/113431
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