Abstract
Methods We isolated T-MSCs from human palatine tonsil and evaluated the ingredients of T-MSCs-CM. The effect of T-MSCs-CM was evaluated in the AR mouse model that was randomly divided into five groups (negative control, positive control, and T-MSCs-CM treated (0.1 mg, 1 mg, and 10 mg)). To investigate the therapeutic effect, we analyzed rhinitis symptoms, serum immunoglobulin (Ig), inflammatory cells, and cytokine expression. We also assessed T cell receptor signal, including MAP kinase (ERK/JNK), p65, and NFAT1. Results We identified the increment of TGF-β1, PGE2, and HGF in the T-MSCs-CM. In an animal study, the T-MSCs-CM-treated group showed significantly reduced allergic symptoms and infiltration of eosinophils and neutrophils in the nasal mucosa, whereas there was no significant difference in total IgE and the OVA-specific IgE level. Additionally, we found that the 10 mg T-MSCs-CM-treated group showed a significantly decreased IL-4 mRNA expression, compared to the (+) Con group. In the analysis of T cell receptor signal, the phosphorylation of MAP kinases, translocation of p65, and activation of NFAT1 were inhibited after T-MSCs-CM. Conclusions Our findings suggest that T-MSCs-CM showed a partial immunomodulatory effect on the AR mouse model by the inhibition of T cell activation via MAP kinase, p65, and NFAT1.
Highlights
Allergic rhinitis (AR) is a common chronic nasal disease presented by the symptoms of sneezing, rhinorrhea, itchiness, and nasal congestion [1]
Based on the surface antigen expression, our findings indicated that the expanded cells included a large population of tonsil-derived mesenchymal stem cells (T-Mesenchymal stem cells (MSCs)), but these cells did not contaminate with the endothelial cell and hematopoietic cell
We found that the concentrations of TGF-β1, prostaglandin E2 (PGE2), and hepatocyte growth factor (HGF) increased more than 200 pg/ml, whereas those of IL-10, nitric oxide (NO), and IDO were negligible
Summary
Allergic rhinitis (AR) is a common chronic nasal disease presented by the symptoms of sneezing, rhinorrhea, itchiness, and nasal congestion [1]. It is characterized by Th2 immune response with an increased influx of eosinophils [1]. The T-MSCs-CM-treated group showed significantly reduced allergic symptoms and infiltration of eosinophils and neutrophils in the nasal mucosa, whereas there was no significant difference in total IgE and the OVA-specific IgE level. Our findings suggest that T-MSCs-CM showed a partial immunomodulatory effect on the AR mouse model by the inhibition of T cell activation via MAP kinase, p65, and NFAT1
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