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Oxidative Stress Enhances the Expression of IL-33 in Airway Epithelial Cells During Virus Infection
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A6353 - Oxidative Stress Enhances the Expression of IL-33 in Airway Epithelial Cells During Virus Infection
Author Block: H. Aizawa1, A. Koarai1, Y. Shishikura1, S. Yanagisawa1, M. Yamaya2, H. Sugiura1, T. Numakura1, M. Yamada1, T. Ichikawa1, N. Fujino1, M. Noda3, Y. Okada3, M. Ichinose1; 1Department of Respiratory Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan, 2Department of Advanced Preventive Medicine for Infectious Disease, Tohoku University Graduate School of Medicine, Sendai, Japan, 3Department of Thoracic Surgery, Institute of Development, Aging and Cancer Tohoku University, Sendai, Japan.
[Rationale and Objectives]
Interleukin-33 (IL-33) is a cytokine belonging to the IL-1 family, and its possible involvement in the pathophysiology of COPD and viral-induced exacerbations has been demonstrated. IL-33 has been shown to be increased in airway epithelial cells from COPD patients, but the regulating mechanism of IL-33 expression in airway epithelial cells remains largely unknown. In the current study, we examined whether oxidative stress, which participates in the pathogenesis of COPD, affects the expression of IL-33 in airway epithelial cells, especially during viral infection.
[Methods]
The effect of hydrogen peroxide (H2O2) on the expression of IL-33, with or without stimulation by polyinosine-polycytidylic acid [poly(I:C)], a synthetic analog of dsRNA that mimics viral infection or rhinovirus infection and its signal pathway, was examined in NCI-H292 cells and primary human bronchial epithelial cells (HBECs) from healthy subjects. In addition, the effect of antioxidant, N-acetylcysteine (NAC) on the expression of IL-33 was compared between HBECs from healthy subjects and those from COPD patients.
[Results]
Treatment with H2O2 significantly potentiated IL-33 expression in NCI-H292 cells, and the potentiation was reversed by NAC treatment. Mitogen-activated protein kinase (MAPK) inhibitors, but not nuclear factor-kappa B inhibitors, also significantly decreased the H2O2-potentiated IL-33 expression. In addition, H2O2 significantly potentiated the poly(I:C)- or rhinovirus-stimulated IL-33 expression. In HBECs from healthy subjects, H2O2-potentiated IL-33 expression and its reversal by NAC was also confirmed. NAC treatment decreased the expression of IL-33 in HBECs from COPD patients, but not in those from healthy subjects.
[Conclusion]
These results demonstrate that oxidative stress is involved in the expression of IL-33 in airway epithelial cells via MAPK signal pathway and it augments IL-33 expression during viral infection. This mechanism may participate in the regulation of IL-33 expression in airway epithelial cells in COPD and in viral-induced exacerbations.
Author Block: H. Aizawa1, A. Koarai1, Y. Shishikura1, S. Yanagisawa1, M. Yamaya2, H. Sugiura1, T. Numakura1, M. Yamada1, T. Ichikawa1, N. Fujino1, M. Noda3, Y. Okada3, M. Ichinose1; 1Department of Respiratory Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan, 2Department of Advanced Preventive Medicine for Infectious Disease, Tohoku University Graduate School of Medicine, Sendai, Japan, 3Department of Thoracic Surgery, Institute of Development, Aging and Cancer Tohoku University, Sendai, Japan.
[Rationale and Objectives]
Interleukin-33 (IL-33) is a cytokine belonging to the IL-1 family, and its possible involvement in the pathophysiology of COPD and viral-induced exacerbations has been demonstrated. IL-33 has been shown to be increased in airway epithelial cells from COPD patients, but the regulating mechanism of IL-33 expression in airway epithelial cells remains largely unknown. In the current study, we examined whether oxidative stress, which participates in the pathogenesis of COPD, affects the expression of IL-33 in airway epithelial cells, especially during viral infection.
[Methods]
The effect of hydrogen peroxide (H2O2) on the expression of IL-33, with or without stimulation by polyinosine-polycytidylic acid [poly(I:C)], a synthetic analog of dsRNA that mimics viral infection or rhinovirus infection and its signal pathway, was examined in NCI-H292 cells and primary human bronchial epithelial cells (HBECs) from healthy subjects. In addition, the effect of antioxidant, N-acetylcysteine (NAC) on the expression of IL-33 was compared between HBECs from healthy subjects and those from COPD patients.
[Results]
Treatment with H2O2 significantly potentiated IL-33 expression in NCI-H292 cells, and the potentiation was reversed by NAC treatment. Mitogen-activated protein kinase (MAPK) inhibitors, but not nuclear factor-kappa B inhibitors, also significantly decreased the H2O2-potentiated IL-33 expression. In addition, H2O2 significantly potentiated the poly(I:C)- or rhinovirus-stimulated IL-33 expression. In HBECs from healthy subjects, H2O2-potentiated IL-33 expression and its reversal by NAC was also confirmed. NAC treatment decreased the expression of IL-33 in HBECs from COPD patients, but not in those from healthy subjects.
[Conclusion]
These results demonstrate that oxidative stress is involved in the expression of IL-33 in airway epithelial cells via MAPK signal pathway and it augments IL-33 expression during viral infection. This mechanism may participate in the regulation of IL-33 expression in airway epithelial cells in COPD and in viral-induced exacerbations.
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