| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2541330 | International Immunopharmacology | 2012 | 7 Pages |
CD4+ T lymphocytes can be primarily polarized to differentiate into Th2 cells, and are heavily involved in the Th2 inflammation of asthma. Little is known about the correlation between microRNAs and Th2 inflammation in asthma, therefore we explore the roles of five microRNAs (microRNA-181a, -155, -150, -146a and -146b) in Th2 inflammation of asthma by tracking their expression levels in splenic CD4+ T lymphocytes under different conditions. Using quantitative real-time polymerase chain reaction (qPCR), the dynamic changes of these microRNAs in murine models of acute asthma (i.e. the OVA group) were analyzed, in comparison to a control group. The effects of dexamethasone on the miRNA expression levels were also investigated. The results showed that the expression levels of microRNA-181a, -150, -146a and -146b were higher in the OVA group compared to the control group in the beginning of the disease, and after 5 days dropped to control group levels because there was no new airway challenge. Moreover, the miRNA-146a expression was down-regulated by treatment with dexamethasone. MicroRNA-181a had a positive linear correlation with the numbers of inflammatory cells (i.e. the numbers of total cells or of the eosinophils in the BALF) by Spearman correlation analysis, so did miRNA-146a and miRNA-146b. These observations suggest that microRNA-181a, -146a and -146b are proinflammatory factors in asthma, and that down-regulation of miRNA-146a may partially account for the anti-inflammatory effect of dexamethasone.
Graphical abstractFigure optionsDownload full-size imageDownload as PowerPoint slideHighlights► MicroRNAs have been reported to participate in immune diseases, such as asthma. ► MicroRNA-181a, -146a and -146b up-regulated in CD4+ T lymphocytes in asthma, acting as proinflammatory factors. ► Dexamethasone could down-regulate the expression of microRNA-146a. ► Up-regulation of these three microRNAs alone was not enough to induce the Th2 inflammation of asthma.
