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KMID : 1130320130560110482
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Korean Journal of Pediatrics
2013 Volume.56 No. 11 p.482 ~ p.489
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The effect of rhinovirus on airway inflammation in a murine asthma model
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Kim Eu-Gene
Lee Hui-Su
Kim Hyun-Sook
Won Sul-Mui
Lee Eu-Kyoung
Kim Hwan-Soo
Bang Kyong-Won
Chun Yoon-Hong
Yoon Jong-Seo
Kim Hyun-Hee
Kim Jin-Tack
Lee Joon-Sung
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Abstract
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Purpose: The aim of the present study was to investigate the differences in lower airway inflammatory
immune responses, including cellular responses and responses in terms of inflammatory mediators in
bronchoalveolar lavage fluid (BALF) and the airway, to rhinovirus (RV) infection on asthma exacerbation
by comparing a control and a murine asthma model, with or without RV infection.
Methods: BALB/c mice were intraperitoneally injected with a crude extract of Dermatophagoides
farinae (Df ) or phosphate buffered saline (PBS) and were subsequently intranasally treated with a
crude extract of Df or PBS. Airway responsiveness and cell infiltration, differential cell counts in BALF,
and cytokine and chemokine concentrations in BALF were measured 24 hours after intranasal RV1B
infection.
Results: RV infection increased the enhanced pause (Penh) in both the Df sensitized and challenged
mice (Df mice) and PBS-treated mice (PBS mice) (P<0.05). Airway eosinophil infiltration increased in
Df mice after RV infection (P<0.05). The levels of interleukin (IL) 13, tumor necrosis factor alpha, and
regulated on activation, normal T cells expressed and secreted (RANTES) increased in response to RV
infection in Df mice, but not in PBS mice (P<0.05). The level of IL-10 significantly decreased following
RV infection in Df mice (P<0.05).
Conclusions: Our findings suggest that the augmented induction of proinflammatory cytokines, Th2
cytokines, and chemokines that mediate an eosinophil response and the decreased induction of
regulatory cytokines after RV infection may be important manifestations leading to airway inflammation
with eosinophil infiltration and changes in airway responsiveness in the asthma model.
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KEYWORD
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Immune response , Rhinovirus , Asthma, Exacerbation
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