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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| Format: | Article |
| Language: | English |
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Wiley
2021-01-01
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| Series: | International Journal of Cell Biology |
| Online Access: | http://dx.doi.org/10.1155/2021/9997625 |
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| author | Manoj J. Mammen Jamil Ali Amita Aurora Umesh C. Sharma Ravikumar Aalinkeel Supriya D. Mahajan Mark Sands Stanley A. Schwartz |
| author_facet | Manoj J. Mammen Jamil Ali Amita Aurora Umesh C. Sharma Ravikumar Aalinkeel Supriya D. Mahajan Mark Sands Stanley A. Schwartz |
| author_sort | Manoj J. Mammen |
| collection | DOAJ |
| 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 Th1/Th2 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. |
| format | Article |
| id | doaj-art-7d6ae9affee34c51a0d15c45db53fa06 |
| institution | Kabale University |
| issn | 1687-8876 1687-8884 |
| language | English |
| publishDate | 2021-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | International Journal of Cell Biology |
| spelling | doaj-art-7d6ae9affee34c51a0d15c45db53fa062025-02-03T01:25:48ZengWileyInternational Journal of Cell Biology1687-88761687-88842021-01-01202110.1155/2021/99976259997625IL-17 Is a Key Regulator of Mucin-Galectin-3 Interactions in AsthmaManoj J. Mammen0Jamil Ali1Amita Aurora2Umesh C. Sharma3Ravikumar Aalinkeel4Supriya D. Mahajan5Mark Sands6Stanley A. Schwartz7Division of Pulmonary, Critical Care & Sleep Medicine, Department of Medicine, State University of New York at Buffalo, 875 Ellicott Street, Buffalo, NY 14203, USADivision of Pulmonary, Critical Care & Sleep Medicine, Department of Medicine, State University of New York at Buffalo, 875 Ellicott Street, Buffalo, NY 14203, USADivision of Pulmonary, Critical Care & Sleep Medicine, Department of Medicine, State University of New York at Buffalo, 875 Ellicott Street, Buffalo, NY 14203, USADivision of Cardiology, Department of Medicine, 875 Ellicott Street, Buffalo, NY 14203, USADivision of Allergy, Immunology & Rheumatology, Department of Medicine, State University of New York at Buffalo, 875 Ellicott Street, Buffalo, NY 14203, USADivision of Allergy, Immunology & Rheumatology, Department of Medicine, State University of New York at Buffalo, 875 Ellicott Street, Buffalo, NY 14203, USADivision of Allergy, Immunology & Rheumatology, Department of Medicine, State University of New York at Buffalo, 875 Ellicott Street, Buffalo, NY 14203, USADivision of Allergy, Immunology & Rheumatology, Department of Medicine, State University of New York at Buffalo, 875 Ellicott Street, Buffalo, NY 14203, USAMucus 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 Th1/Th2 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.http://dx.doi.org/10.1155/2021/9997625 |
| spellingShingle | Manoj J. Mammen Jamil Ali Amita Aurora Umesh C. Sharma Ravikumar Aalinkeel Supriya D. Mahajan Mark Sands Stanley A. Schwartz IL-17 Is a Key Regulator of Mucin-Galectin-3 Interactions in Asthma International Journal of Cell Biology |
| 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 |
| url | http://dx.doi.org/10.1155/2021/9997625 |
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