Regulation of IL-33 by Oncostatin M in Mouse Lung Epithelial Cells
IL-33 modulates both innate and adaptive immune responses at tissue sites including lung and may play critical roles in inflammatory lung disease. Although IL-33 expression can be altered upon NF-Kappa B activation, here we examine regulation by Oncostatin M, a gp130 cytokine family member, in mouse...
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Format: | Article |
Language: | English |
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Wiley
2016-01-01
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Series: | Mediators of Inflammation |
Online Access: | http://dx.doi.org/10.1155/2016/9858374 |
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author | Carl D. Richards Laura Izakelian Anisha Dubey Grace Zhang Steven Wong Karen Kwofie Aatif Qureshi Fernando Botelho |
author_facet | Carl D. Richards Laura Izakelian Anisha Dubey Grace Zhang Steven Wong Karen Kwofie Aatif Qureshi Fernando Botelho |
author_sort | Carl D. Richards |
collection | DOAJ |
description | IL-33 modulates both innate and adaptive immune responses at tissue sites including lung and may play critical roles in inflammatory lung disease. Although IL-33 expression can be altered upon NF-Kappa B activation, here we examine regulation by Oncostatin M, a gp130 cytokine family member, in mouse lung tissue. Responses were assessed in BALB/c mouse lung at day 7 of transient overexpression using endotracheally administered adenovirus encoding OSM (AdOSM) or empty vector (AdDel70). Whole lung extracts showed induction of IL-33 mRNA (>20-fold) and protein (10-fold increase in immunoblots) by AdOSM relative to AdDel70. Immunohistochemistry for IL-33 indicated a marked induction of nuclear staining in alveolar epithelial cells in vivo. Oncostatin M stimulated IL-33 mRNA and IL-33 full length protein in C10 mouse type 2 alveolar epithelial cells in culture in time-dependent and dose-dependent fashion, whereas IL-6, LIF, IL-31, IL-4, or IL-13 did not, and TGFβ repressed IL-33. IL-33 induction was associated with activation of STAT3, and pharmacological inhibition of STAT3 ameliorated IL-33 levels. These results indicate Oncostatin M as a potent inducer of IL-33 in mouse lung epithelial cells and suggest that an OSM/IL-33 axis may participate in innate immunity and inflammatory conditions in lung. |
format | Article |
id | doaj-art-92cb882255df45918a2ae4f4d48c41ea |
institution | Kabale University |
issn | 0962-9351 1466-1861 |
language | English |
publishDate | 2016-01-01 |
publisher | Wiley |
record_format | Article |
series | Mediators of Inflammation |
spelling | doaj-art-92cb882255df45918a2ae4f4d48c41ea2025-02-03T06:13:06ZengWileyMediators of Inflammation0962-93511466-18612016-01-01201610.1155/2016/98583749858374Regulation of IL-33 by Oncostatin M in Mouse Lung Epithelial CellsCarl D. Richards0Laura Izakelian1Anisha Dubey2Grace Zhang3Steven Wong4Karen Kwofie5Aatif Qureshi6Fernando Botelho7McMaster Immunology Research Centre, Department of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, CanadaMcMaster Immunology Research Centre, Department of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, CanadaMcMaster Immunology Research Centre, Department of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, CanadaMcMaster Immunology Research Centre, Department of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, CanadaMcMaster Immunology Research Centre, Department of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, CanadaMcMaster Immunology Research Centre, Department of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, CanadaMcMaster Immunology Research Centre, Department of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, CanadaMcMaster Immunology Research Centre, Department of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, CanadaIL-33 modulates both innate and adaptive immune responses at tissue sites including lung and may play critical roles in inflammatory lung disease. Although IL-33 expression can be altered upon NF-Kappa B activation, here we examine regulation by Oncostatin M, a gp130 cytokine family member, in mouse lung tissue. Responses were assessed in BALB/c mouse lung at day 7 of transient overexpression using endotracheally administered adenovirus encoding OSM (AdOSM) or empty vector (AdDel70). Whole lung extracts showed induction of IL-33 mRNA (>20-fold) and protein (10-fold increase in immunoblots) by AdOSM relative to AdDel70. Immunohistochemistry for IL-33 indicated a marked induction of nuclear staining in alveolar epithelial cells in vivo. Oncostatin M stimulated IL-33 mRNA and IL-33 full length protein in C10 mouse type 2 alveolar epithelial cells in culture in time-dependent and dose-dependent fashion, whereas IL-6, LIF, IL-31, IL-4, or IL-13 did not, and TGFβ repressed IL-33. IL-33 induction was associated with activation of STAT3, and pharmacological inhibition of STAT3 ameliorated IL-33 levels. These results indicate Oncostatin M as a potent inducer of IL-33 in mouse lung epithelial cells and suggest that an OSM/IL-33 axis may participate in innate immunity and inflammatory conditions in lung.http://dx.doi.org/10.1155/2016/9858374 |
spellingShingle | Carl D. Richards Laura Izakelian Anisha Dubey Grace Zhang Steven Wong Karen Kwofie Aatif Qureshi Fernando Botelho Regulation of IL-33 by Oncostatin M in Mouse Lung Epithelial Cells Mediators of Inflammation |
title | Regulation of IL-33 by Oncostatin M in Mouse Lung Epithelial Cells |
title_full | Regulation of IL-33 by Oncostatin M in Mouse Lung Epithelial Cells |
title_fullStr | Regulation of IL-33 by Oncostatin M in Mouse Lung Epithelial Cells |
title_full_unstemmed | Regulation of IL-33 by Oncostatin M in Mouse Lung Epithelial Cells |
title_short | Regulation of IL-33 by Oncostatin M in Mouse Lung Epithelial Cells |
title_sort | regulation of il 33 by oncostatin m in mouse lung epithelial cells |
url | http://dx.doi.org/10.1155/2016/9858374 |
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