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IL-17 Is a Key Regulator of Mucin-Galectin-3 Interactions in Asthma

Mucus hypersecretion and chronic airway inflammation are standard characteristics of several airway diseases, such as chronic obstructive pulmonary disease and asthma. Increased mucus secretion from increased mucin gene expression in the airway epithelium is associated with poor prognosis and mortal...

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Autores principales: Mammen, Manoj J., Ali, Jamil, Aurora, Amita, Sharma, Umesh C., Aalinkeel, Ravikumar, Mahajan, Supriya D., Sands, Mark, Schwartz, Stanley A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8211528/
https://www.ncbi.nlm.nih.gov/pubmed/34221020
http://dx.doi.org/10.1155/2021/9997625
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author Mammen, Manoj J.
Ali, Jamil
Aurora, Amita
Sharma, Umesh C.
Aalinkeel, Ravikumar
Mahajan, Supriya D.
Sands, Mark
Schwartz, Stanley A.
author_facet Mammen, Manoj J.
Ali, Jamil
Aurora, Amita
Sharma, Umesh C.
Aalinkeel, Ravikumar
Mahajan, Supriya D.
Sands, Mark
Schwartz, Stanley A.
author_sort Mammen, Manoj J.
collection PubMed
description Mucus hypersecretion and chronic airway inflammation are standard characteristics of several airway diseases, such as chronic obstructive pulmonary disease and asthma. Increased mucus secretion from increased mucin gene expression in the airway epithelium is associated with poor prognosis and mortality. We previously showed that the absence of tissue inhibitor of metalloproteinase 1 (TIMP-1) enhances lung inflammation, airway hyperreactivity, and lung remodeling in asthma in an ovalbumin (OVA) asthma model of TIMP-1 knockout (TIMPKO) mice as compared to wild-type (WT) controls and mediated by increased galectin-3 (Gal-3) levels. Additionally, we have shown that in the lung epithelial cell line A549, Gal-3 inhibition increases interleukin-17 (IL-17) levels, leading to increased mucin expression in the airway epithelium. Therefore, in the current study, we further examined the relationship between Gal-3 and the production of IL-17-axis cytokines and critical members of the mucin family in the murine TIMPKO asthma model and the lung epithelium cell line A549. While Gal-3 may regulate a Th(1)/Th(2) response, IL-17 could stimulate the mucin genes, MUC5B and MUC5AC. Gal-3 and IL-17 interactions induce mucus expression in OVA-sensitized mice. We conclude that Gal-3 may play an essential role in the pathogenesis of asthma, and modulation of Gal-3 may prove helpful in the treatment of this disease.
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spelling pubmed-82115282021-07-01 IL-17 Is a Key Regulator of Mucin-Galectin-3 Interactions in Asthma Mammen, Manoj J. Ali, Jamil Aurora, Amita Sharma, Umesh C. Aalinkeel, Ravikumar Mahajan, Supriya D. Sands, Mark Schwartz, Stanley A. Int J Cell Biol Research Article Mucus hypersecretion and chronic airway inflammation are standard characteristics of several airway diseases, such as chronic obstructive pulmonary disease and asthma. Increased mucus secretion from increased mucin gene expression in the airway epithelium is associated with poor prognosis and mortality. We previously showed that the absence of tissue inhibitor of metalloproteinase 1 (TIMP-1) enhances lung inflammation, airway hyperreactivity, and lung remodeling in asthma in an ovalbumin (OVA) asthma model of TIMP-1 knockout (TIMPKO) mice as compared to wild-type (WT) controls and mediated by increased galectin-3 (Gal-3) levels. Additionally, we have shown that in the lung epithelial cell line A549, Gal-3 inhibition increases interleukin-17 (IL-17) levels, leading to increased mucin expression in the airway epithelium. Therefore, in the current study, we further examined the relationship between Gal-3 and the production of IL-17-axis cytokines and critical members of the mucin family in the murine TIMPKO asthma model and the lung epithelium cell line A549. While Gal-3 may regulate a Th(1)/Th(2) response, IL-17 could stimulate the mucin genes, MUC5B and MUC5AC. Gal-3 and IL-17 interactions induce mucus expression in OVA-sensitized mice. We conclude that Gal-3 may play an essential role in the pathogenesis of asthma, and modulation of Gal-3 may prove helpful in the treatment of this disease. Hindawi 2021-06-09 /pmc/articles/PMC8211528/ /pubmed/34221020 http://dx.doi.org/10.1155/2021/9997625 Text en Copyright © 2021 Manoj J. Mammen et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Mammen, Manoj J.
Ali, Jamil
Aurora, Amita
Sharma, Umesh C.
Aalinkeel, Ravikumar
Mahajan, Supriya D.
Sands, Mark
Schwartz, Stanley A.
IL-17 Is a Key Regulator of Mucin-Galectin-3 Interactions in Asthma
title IL-17 Is a Key Regulator of Mucin-Galectin-3 Interactions in Asthma
title_full IL-17 Is a Key Regulator of Mucin-Galectin-3 Interactions in Asthma
title_fullStr IL-17 Is a Key Regulator of Mucin-Galectin-3 Interactions in Asthma
title_full_unstemmed IL-17 Is a Key Regulator of Mucin-Galectin-3 Interactions in Asthma
title_short IL-17 Is a Key Regulator of Mucin-Galectin-3 Interactions in Asthma
title_sort il-17 is a key regulator of mucin-galectin-3 interactions in asthma
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8211528/
https://www.ncbi.nlm.nih.gov/pubmed/34221020
http://dx.doi.org/10.1155/2021/9997625
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