Autocrine Acetylcholine, Induced by IL-17A via NFκB and ERK1/2 Pathway Activation, Promotes MUC5AC and IL-8 Synthesis in Bronchial Epithelial Cells
IL-17A is overexpressed in the lung during acute neutrophilic inflammation. Acetylcholine (ACh) increases IL-8 and Muc5AC production in airway epithelial cells. We aimed to characterize the involvement of nonneuronal components of cholinergic system on IL-8 and Muc5AC production in bronchial epithel...
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| Main Authors: | , , , , , , , , , , , |
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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/10.1155/2016/9063842 |
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| author | Angela Marina Montalbano Giusy Daniela Albano Anna Bonanno Loredana Riccobono Caterina Di Sano Maria Ferraro Liboria Siena Giulia Anzalone Rosalia Gagliardo Michael Paul Pieper Mark Gjomarkaj Mirella Profita |
| author_facet | Angela Marina Montalbano Giusy Daniela Albano Anna Bonanno Loredana Riccobono Caterina Di Sano Maria Ferraro Liboria Siena Giulia Anzalone Rosalia Gagliardo Michael Paul Pieper Mark Gjomarkaj Mirella Profita |
| author_sort | Angela Marina Montalbano |
| collection | DOAJ |
| description | IL-17A is overexpressed in the lung during acute neutrophilic inflammation. Acetylcholine (ACh) increases IL-8 and Muc5AC production in airway epithelial cells. We aimed to characterize the involvement of nonneuronal components of cholinergic system on IL-8 and Muc5AC production in bronchial epithelial cells stimulated with IL-17A. Bronchial epithelial cells were stimulated with recombinant human IL-17A (rhIL-17A) to evaluate the ChAT expression, the ACh binding and production, the IL-8 release, and the Muc5AC production. Furthermore, the effectiveness of PD098,059 (inhibitor of MAPKK activation), Bay11-7082 (inhibitor of IkBα phosphorylation), Hemicholinium-3 (HCh-3) (choline uptake blocker), and Tiotropium bromide (Spiriva®) (anticholinergic drug) was tested in our in vitro model. We showed that rhIL-17A increased the expression of ChAT, the levels of ACh binding and production, and the IL-8 and Muc5AC production in stimulated bronchial epithelial cells compared with untreated cells. The pretreatment of the cells with PD098,059 and Bay11-7082 decreased the ChAT expression and the ACh production/binding, while HCh-3 and Tiotropium decreased the IL-8 and Muc5AC synthesis in bronchial epithelial cells stimulated with rhIL-17A. IL-17A is involved in the IL-8 and Muc5AC production promoting, via NFκB and ERK1/2 pathway activation, the synthesis of ChAT, and the related activity of autocrine ACh in bronchial epithelial cells. |
| format | Article |
| id | doaj-art-484f7845abd14b50bf92bdd9ee189963 |
| 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-484f7845abd14b50bf92bdd9ee1899632025-02-03T01:27:12ZengWileyMediators of Inflammation0962-93511466-18612016-01-01201610.1155/2016/90638429063842Autocrine Acetylcholine, Induced by IL-17A via NFκB and ERK1/2 Pathway Activation, Promotes MUC5AC and IL-8 Synthesis in Bronchial Epithelial CellsAngela Marina Montalbano0Giusy Daniela Albano1Anna Bonanno2Loredana Riccobono3Caterina Di Sano4Maria Ferraro5Liboria Siena6Giulia Anzalone7Rosalia Gagliardo8Michael Paul Pieper9Mark Gjomarkaj10Mirella Profita11Institute of Biomedicine and Molecular Immunology “A. Monroy” (IBIM), National Research Council of Italy (CNR), 90146 Palermo, ItalyInstitute of Biomedicine and Molecular Immunology “A. Monroy” (IBIM), National Research Council of Italy (CNR), 90146 Palermo, ItalyInstitute of Biomedicine and Molecular Immunology “A. Monroy” (IBIM), National Research Council of Italy (CNR), 90146 Palermo, ItalyInstitute of Biomedicine and Molecular Immunology “A. Monroy” (IBIM), National Research Council of Italy (CNR), 90146 Palermo, ItalyInstitute of Biomedicine and Molecular Immunology “A. Monroy” (IBIM), National Research Council of Italy (CNR), 90146 Palermo, ItalyInstitute of Biomedicine and Molecular Immunology “A. Monroy” (IBIM), National Research Council of Italy (CNR), 90146 Palermo, ItalyInstitute of Biomedicine and Molecular Immunology “A. Monroy” (IBIM), National Research Council of Italy (CNR), 90146 Palermo, ItalyInstitute of Biomedicine and Molecular Immunology “A. Monroy” (IBIM), National Research Council of Italy (CNR), 90146 Palermo, ItalyInstitute of Biomedicine and Molecular Immunology “A. Monroy” (IBIM), National Research Council of Italy (CNR), 90146 Palermo, ItalyBoehringer Ingelheim Pharma GmbH & Co. KG, 88400 Biberach, GermanyInstitute of Biomedicine and Molecular Immunology “A. Monroy” (IBIM), National Research Council of Italy (CNR), 90146 Palermo, ItalyInstitute of Biomedicine and Molecular Immunology “A. Monroy” (IBIM), National Research Council of Italy (CNR), 90146 Palermo, ItalyIL-17A is overexpressed in the lung during acute neutrophilic inflammation. Acetylcholine (ACh) increases IL-8 and Muc5AC production in airway epithelial cells. We aimed to characterize the involvement of nonneuronal components of cholinergic system on IL-8 and Muc5AC production in bronchial epithelial cells stimulated with IL-17A. Bronchial epithelial cells were stimulated with recombinant human IL-17A (rhIL-17A) to evaluate the ChAT expression, the ACh binding and production, the IL-8 release, and the Muc5AC production. Furthermore, the effectiveness of PD098,059 (inhibitor of MAPKK activation), Bay11-7082 (inhibitor of IkBα phosphorylation), Hemicholinium-3 (HCh-3) (choline uptake blocker), and Tiotropium bromide (Spiriva®) (anticholinergic drug) was tested in our in vitro model. We showed that rhIL-17A increased the expression of ChAT, the levels of ACh binding and production, and the IL-8 and Muc5AC production in stimulated bronchial epithelial cells compared with untreated cells. The pretreatment of the cells with PD098,059 and Bay11-7082 decreased the ChAT expression and the ACh production/binding, while HCh-3 and Tiotropium decreased the IL-8 and Muc5AC synthesis in bronchial epithelial cells stimulated with rhIL-17A. IL-17A is involved in the IL-8 and Muc5AC production promoting, via NFκB and ERK1/2 pathway activation, the synthesis of ChAT, and the related activity of autocrine ACh in bronchial epithelial cells.http://dx.doi.org/10.1155/2016/9063842 |
| spellingShingle | Angela Marina Montalbano Giusy Daniela Albano Anna Bonanno Loredana Riccobono Caterina Di Sano Maria Ferraro Liboria Siena Giulia Anzalone Rosalia Gagliardo Michael Paul Pieper Mark Gjomarkaj Mirella Profita Autocrine Acetylcholine, Induced by IL-17A via NFκB and ERK1/2 Pathway Activation, Promotes MUC5AC and IL-8 Synthesis in Bronchial Epithelial Cells Mediators of Inflammation |
| title | Autocrine Acetylcholine, Induced by IL-17A via NFκB and ERK1/2 Pathway Activation, Promotes MUC5AC and IL-8 Synthesis in Bronchial Epithelial Cells |
| title_full | Autocrine Acetylcholine, Induced by IL-17A via NFκB and ERK1/2 Pathway Activation, Promotes MUC5AC and IL-8 Synthesis in Bronchial Epithelial Cells |
| title_fullStr | Autocrine Acetylcholine, Induced by IL-17A via NFκB and ERK1/2 Pathway Activation, Promotes MUC5AC and IL-8 Synthesis in Bronchial Epithelial Cells |
| title_full_unstemmed | Autocrine Acetylcholine, Induced by IL-17A via NFκB and ERK1/2 Pathway Activation, Promotes MUC5AC and IL-8 Synthesis in Bronchial Epithelial Cells |
| title_short | Autocrine Acetylcholine, Induced by IL-17A via NFκB and ERK1/2 Pathway Activation, Promotes MUC5AC and IL-8 Synthesis in Bronchial Epithelial Cells |
| title_sort | autocrine acetylcholine induced by il 17a via nfκb and erk1 2 pathway activation promotes muc5ac and il 8 synthesis in bronchial epithelial cells |
| url | http://dx.doi.org/10.1155/2016/9063842 |
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