Th17 cytokines induce pro-fibrotic cytokines release from human eosinophils View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2013-12

AUTHORS

Saleh Al-Muhsen, Severine Letuve, Alejandro Vazquez-Tello, Mary Angeline Pureza, Hamdan Al-Jahdali, Ahmed S Bahammam, Qutayba Hamid, Rabih Halwani

ABSTRACT

BACKGROUND: Subepithelial fibrosis is one of the most critical structural changes affecting bronchial airway function during asthma. Eosinophils have been shown to contribute to the production of pro-fibrotic cytokines, TGF-β and IL-11, however, the mechanism regulating this process is not fully understood. OBJECTIVE: In this report, we investigated whether cytokines associated with inflammation during asthma may induce eosinophils to produce pro-fibrotic cytokines. METHODS: Eosinophils were isolated from peripheral blood of 10 asthmatics and 10 normal control subjects. Eosinophils were stimulated with Th1, Th2 and Th17 cytokines and the production of TGF-β and IL-11 was determined using real time PCR and ELISA assays. RESULTS: The basal expression levels of eosinophil derived TGF-β and IL-11 cytokines were comparable between asthmatic and healthy individuals. Stimulating eosinophils with Th1 and Th2 cytokines did not induce expression of pro-fibrotic cytokines. However, stimulating eosinophils with Th17 cytokines resulted in the enhancement of TGF-β and IL-11 expression in asthmatic but not healthy individuals. This effect of IL-17 on eosinophils was dependent on p38 MAPK activation as inhibiting the phosphorylation of p38 MAPK, but not other kinases, inhibited IL-17 induced pro-fibrotic cytokine release. CONCLUSIONS: Th17 cytokines might contribute to airway fibrosis during asthma by enhancing production of eosinophil derived pro-fibrotic cytokines. Preventing the release of pro-fibrotic cytokines by blocking the effect of Th17 cytokines on eosinophils may prove to be beneficial in controlling fibrosis for disorders with IL-17 driven inflammation such as allergic and autoimmune diseases. More... »

PAGES

34

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/1465-9921-14-34

DOI

http://dx.doi.org/10.1186/1465-9921-14-34

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1017944562

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/23496774


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