Abstract
Background Allergic rhinitis (AR) is a global disease without specific treatment. Human mesenchymal stem cell- (HMSC-) derived exosomes (HMSC-exos) have been implicated for the amelioration of allergic inflammation by delivering miR-146a-5p in a mouse asthma model. However, the antiallergic activity and the underlying mechanism of HMSC-exos in AR remain unclear. The present study aimed to investigate the role of HMSC-exos in the pathogenesis of AR. Materials and Methods Blood specimens were collected from AR patients and healthy donators for investigation. HMSC and CD4+ T cells were used in the present study. Flow cytometry was used to characterize the population of Type 1 helper T (Th1) and Th2 cells. Specific siRNA and overexpressed plasmids were designed to silence or overexpress the expressions of miR-146a-5p and SERPINB2. Luciferase reporter assay was adopted to explore the binding site of miR-146a-5p and SERPINB2. Quantitative real-time PCR and immunoblots were performed to estimate the expression of target genes. Results The population of Th2 cells was significantly elevated in AR patients as compared with that in healthy donators. HMSC-exos could decrease the expression of SERPINB2 and the differentiation of Th2 cells. miR-146a-5p in HMSC-exos exhibited consistent effects and lowered the expression of SERPINB2 by binding on its 3′UTR region. Moreover, the differentiation of Th2 cells was promoted by SERPINB2 that could be reversed by HMSC-exos. Additionally, the miR-146a-5p expression was negatively associated with the SERPINB2 expression in the serum of AR patients. Conclusion HMSC-exos could inhibit the differentiation of Th2 cells via the regulation of the miR-146a-5p/SERPINB2 pathway. miR-146a-5p and SERPINB2 could be applied as potential targets for AR treatment.
Highlights
Allergic rhinitis (AR) is a type of nasal mucosal disease characterized by overreacted immune responses
Flow cytometry showed that the quantity of Th1 (CD4+IFN-γ+) was significantly decreased, whereas that of Th2 (CD4+IL-4+) was significantly increased in AR patients as compared with that in healthy donators (p < 0:05) (Figure 1(a))
The population of Th1 cells did not change significantly, whereas that of Th2 cells decreased significantly after coculture with Human mesenchymal stem cell- (HMSC-)exos (p < 0:05) (Figure 7(c)). These results indicated that SERPINB2 could promote the differentiation of Th2 cells, which was suppressed by human mesenchymal stem cell (HMSC)-exos
Summary
Allergic rhinitis (AR) is a type of nasal mucosal disease characterized by overreacted immune responses. Allergic rhinitis (AR) is a global disease without specific treatment. Human mesenchymal stem cell- (HMSC-) derived exosomes (HMSC-exos) have been implicated for the amelioration of allergic inflammation by delivering miR-146a-5p in a mouse asthma model. The present study aimed to investigate the role of HMSC-exos in the pathogenesis of AR. The population of Th2 cells was significantly elevated in AR patients as compared with that in healthy donators. HMSC-exos could decrease the expression of SERPINB2 and the differentiation of Th2 cells. MiR-146a-5p in HMSC-exos exhibited consistent effects and lowered the expression of SERPINB2 by binding on its 3′UTR region. The differentiation of Th2 cells was promoted by SERPINB2 that could be reversed by HMSC-exos. HMSC-exos could inhibit the differentiation of Th2 cells via the regulation of the miR146a-5p/SERPINB2 pathway. HMSC-exos could inhibit the differentiation of Th2 cells via the regulation of the miR146a-5p/SERPINB2 pathway. miR-146a-5p and SERPINB2 could be applied as potential targets for AR treatment
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