Pandemic influenza virus, pH1N1, induces asthmatic symptoms via activation of innate lymphoid cells

D. H. Shim, Y. A. Park, M. J. Kim, J. Y. Hong, J. Y. Baek, K. W. Kim, Y. H. Byun, Baik Lin Seong, S. Ryu, M. K. Song, K. J. Hong, W. Na, D. Song, J. H. Park, M. H. Sohn, J. M. Lee

Research output: Contribution to journalArticle

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Abstract

Background: The pandemic strain of the influenza A virus (pH1N1) in 2009 caused many complications in patients. In this study, we introduce asthmatic symptoms as a complication of pH1N1 infection in children, not having a relationship with asthma history. The aim of this study was to quantify asthmatic symptoms in pH1N1-infected children and elucidate the underlying mechanisms of airway hyper-responsiveness (AHR) induced in a murine model of pH1N1 infection. Methods: As a retrospective study, pH1N1-infected children who were hospitalized with moderate to severe acute asthmatic symptoms were enrolled and administered a methacholine challenge test (MCT) at 3 months post-discharge. Additionally, the induction of AHR by pH1N1 infection was measured by MCT in wild-type and Rag1-/- mice. The effect of the innate immune response on the development of AHR following pH1N1 infection was investigated. Results: More than 70% of the pH1N1-infected children without a pre-infection diagnosis of asthma had a negative response on the MCT. None of these children had recurrent wheezing or asthma during the 3 years following pH1N1 infection. The development of AHR in pH1N1-infected mice was associated with an elevation in IL-33 and innate lymphoid cells 2 (ILC2). Conclusions: This study demonstrates that pH1N1 infection directly induces transient asthmatic symptoms in patients regardless of their medical history. pH1N1 infection was shown to stimulate the rapid development of AHR and Th2-type cytokine secretion in mice via the activation of ILC2; it may be activated independently of adaptive immunity.

Original languageEnglish
Pages (from-to)780-788
Number of pages9
JournalPediatric Allergy and Immunology
Volume26
Issue number8
DOIs
Publication statusPublished - 2015 Dec 1

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Respiratory Hypersensitivity
Pandemics
Orthomyxoviridae
Lymphocytes
Infection
Methacholine Chloride
Asthma
Influenza A virus
Respiratory Sounds
Adaptive Immunity
Innate Immunity
Retrospective Studies
Cytokines

All Science Journal Classification (ASJC) codes

  • Pediatrics, Perinatology, and Child Health
  • Immunology and Allergy
  • Immunology

Cite this

Shim, D. H., Park, Y. A., Kim, M. J., Hong, J. Y., Baek, J. Y., Kim, K. W., ... Lee, J. M. (2015). Pandemic influenza virus, pH1N1, induces asthmatic symptoms via activation of innate lymphoid cells. Pediatric Allergy and Immunology, 26(8), 780-788. https://doi.org/10.1111/pai.12462
Shim, D. H. ; Park, Y. A. ; Kim, M. J. ; Hong, J. Y. ; Baek, J. Y. ; Kim, K. W. ; Byun, Y. H. ; Seong, Baik Lin ; Ryu, S. ; Song, M. K. ; Hong, K. J. ; Na, W. ; Song, D. ; Park, J. H. ; Sohn, M. H. ; Lee, J. M. / Pandemic influenza virus, pH1N1, induces asthmatic symptoms via activation of innate lymphoid cells. In: Pediatric Allergy and Immunology. 2015 ; Vol. 26, No. 8. pp. 780-788.
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abstract = "Background: The pandemic strain of the influenza A virus (pH1N1) in 2009 caused many complications in patients. In this study, we introduce asthmatic symptoms as a complication of pH1N1 infection in children, not having a relationship with asthma history. The aim of this study was to quantify asthmatic symptoms in pH1N1-infected children and elucidate the underlying mechanisms of airway hyper-responsiveness (AHR) induced in a murine model of pH1N1 infection. Methods: As a retrospective study, pH1N1-infected children who were hospitalized with moderate to severe acute asthmatic symptoms were enrolled and administered a methacholine challenge test (MCT) at 3 months post-discharge. Additionally, the induction of AHR by pH1N1 infection was measured by MCT in wild-type and Rag1-/- mice. The effect of the innate immune response on the development of AHR following pH1N1 infection was investigated. Results: More than 70{\%} of the pH1N1-infected children without a pre-infection diagnosis of asthma had a negative response on the MCT. None of these children had recurrent wheezing or asthma during the 3 years following pH1N1 infection. The development of AHR in pH1N1-infected mice was associated with an elevation in IL-33 and innate lymphoid cells 2 (ILC2). Conclusions: This study demonstrates that pH1N1 infection directly induces transient asthmatic symptoms in patients regardless of their medical history. pH1N1 infection was shown to stimulate the rapid development of AHR and Th2-type cytokine secretion in mice via the activation of ILC2; it may be activated independently of adaptive immunity.",
author = "Shim, {D. H.} and Park, {Y. A.} and Kim, {M. J.} and Hong, {J. Y.} and Baek, {J. Y.} and Kim, {K. W.} and Byun, {Y. H.} and Seong, {Baik Lin} and S. Ryu and Song, {M. K.} and Hong, {K. J.} and W. Na and D. Song and Park, {J. H.} and Sohn, {M. H.} and Lee, {J. M.}",
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Shim, DH, Park, YA, Kim, MJ, Hong, JY, Baek, JY, Kim, KW, Byun, YH, Seong, BL, Ryu, S, Song, MK, Hong, KJ, Na, W, Song, D, Park, JH, Sohn, MH & Lee, JM 2015, 'Pandemic influenza virus, pH1N1, induces asthmatic symptoms via activation of innate lymphoid cells', Pediatric Allergy and Immunology, vol. 26, no. 8, pp. 780-788. https://doi.org/10.1111/pai.12462

Pandemic influenza virus, pH1N1, induces asthmatic symptoms via activation of innate lymphoid cells. / Shim, D. H.; Park, Y. A.; Kim, M. J.; Hong, J. Y.; Baek, J. Y.; Kim, K. W.; Byun, Y. H.; Seong, Baik Lin; Ryu, S.; Song, M. K.; Hong, K. J.; Na, W.; Song, D.; Park, J. H.; Sohn, M. H.; Lee, J. M.

In: Pediatric Allergy and Immunology, Vol. 26, No. 8, 01.12.2015, p. 780-788.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Pandemic influenza virus, pH1N1, induces asthmatic symptoms via activation of innate lymphoid cells

AU - Shim, D. H.

AU - Park, Y. A.

AU - Kim, M. J.

AU - Hong, J. Y.

AU - Baek, J. Y.

AU - Kim, K. W.

AU - Byun, Y. H.

AU - Seong, Baik Lin

AU - Ryu, S.

AU - Song, M. K.

AU - Hong, K. J.

AU - Na, W.

AU - Song, D.

AU - Park, J. H.

AU - Sohn, M. H.

AU - Lee, J. M.

PY - 2015/12/1

Y1 - 2015/12/1

N2 - Background: The pandemic strain of the influenza A virus (pH1N1) in 2009 caused many complications in patients. In this study, we introduce asthmatic symptoms as a complication of pH1N1 infection in children, not having a relationship with asthma history. The aim of this study was to quantify asthmatic symptoms in pH1N1-infected children and elucidate the underlying mechanisms of airway hyper-responsiveness (AHR) induced in a murine model of pH1N1 infection. Methods: As a retrospective study, pH1N1-infected children who were hospitalized with moderate to severe acute asthmatic symptoms were enrolled and administered a methacholine challenge test (MCT) at 3 months post-discharge. Additionally, the induction of AHR by pH1N1 infection was measured by MCT in wild-type and Rag1-/- mice. The effect of the innate immune response on the development of AHR following pH1N1 infection was investigated. Results: More than 70% of the pH1N1-infected children without a pre-infection diagnosis of asthma had a negative response on the MCT. None of these children had recurrent wheezing or asthma during the 3 years following pH1N1 infection. The development of AHR in pH1N1-infected mice was associated with an elevation in IL-33 and innate lymphoid cells 2 (ILC2). Conclusions: This study demonstrates that pH1N1 infection directly induces transient asthmatic symptoms in patients regardless of their medical history. pH1N1 infection was shown to stimulate the rapid development of AHR and Th2-type cytokine secretion in mice via the activation of ILC2; it may be activated independently of adaptive immunity.

AB - Background: The pandemic strain of the influenza A virus (pH1N1) in 2009 caused many complications in patients. In this study, we introduce asthmatic symptoms as a complication of pH1N1 infection in children, not having a relationship with asthma history. The aim of this study was to quantify asthmatic symptoms in pH1N1-infected children and elucidate the underlying mechanisms of airway hyper-responsiveness (AHR) induced in a murine model of pH1N1 infection. Methods: As a retrospective study, pH1N1-infected children who were hospitalized with moderate to severe acute asthmatic symptoms were enrolled and administered a methacholine challenge test (MCT) at 3 months post-discharge. Additionally, the induction of AHR by pH1N1 infection was measured by MCT in wild-type and Rag1-/- mice. The effect of the innate immune response on the development of AHR following pH1N1 infection was investigated. Results: More than 70% of the pH1N1-infected children without a pre-infection diagnosis of asthma had a negative response on the MCT. None of these children had recurrent wheezing or asthma during the 3 years following pH1N1 infection. The development of AHR in pH1N1-infected mice was associated with an elevation in IL-33 and innate lymphoid cells 2 (ILC2). Conclusions: This study demonstrates that pH1N1 infection directly induces transient asthmatic symptoms in patients regardless of their medical history. pH1N1 infection was shown to stimulate the rapid development of AHR and Th2-type cytokine secretion in mice via the activation of ILC2; it may be activated independently of adaptive immunity.

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