Abstract
Olfactory ecto-mesenchymal stem cells (OE-MSCs) are a novel population of resident stem cells in the olfactory lamina propria with strong immunosuppressive function. Exosomes released by MSCs are considered to carry various mRNAs, microRNAs and proteins from cells and function as an extension of MSCs. However, it remains unclear whether exosomes derived from OE-MSCs (OE-MSCs-Exos) possess any immunoregulatory functions. In this study, we found that OE-MSCs-Exos possessed strong suppressive function in CD4+T cell proliferation, accompanied by reduced IL-17, IFN-γ and enhanced TGF-β, IL-10 secreted by T cells. In experimental colitis mice, treatment of OE-MSCs-Exos markedly alleviated the severity of disease, and Th1/Th17 subpopulations were remarkably reduced whereas Treg cells were increased after OE-MSCs-Exos treatment. Mechanistically, OE-MSCs-Exos were demonstrated to inhibit the differentiation of Th1 and Th17 cells, but promote the induction of Treg cells in vitro. Taken together, our findings identified a novel function of OE-MSCs-Exos in regulating T-cell responses, indicating that OE-MSCs-Exos may represent a new cell-free therapy for the treatment of IBD and other inflammatory diseases.
Highlights
Inflammatory bowel disease (IBD) is a chronic, relapsing, and remitting inflammatory disorder of intestinal tract, including Crohn’s disease and ulcerative colitis
We first showed the typical Mesenchymal stem cells (MSCs) phenotypic markers on Olfactory ecto-mesenchymal stem cells (OE-MSCs), and the capability of differentiating into osteocytes and adipocytes further confirmed they were of stem cell property
Afterwards, adoptive transfer of OEMSCs-Exos exhibited obvious therapeutic effect in the experimental colitis mice, both Th1 and Th17 cell responses were suppressed while Treg cells were expanded after OE-MSCs
Summary
Inflammatory bowel disease (IBD) is a chronic, relapsing, and remitting inflammatory disorder of intestinal tract, including Crohn’s disease and ulcerative colitis. The incidence of IBD has increased worldwide and challenges the public health [1]. It has been acknowledged that the long-term chronic inflammation in the intestine can cause abscesses, fistulas, extraintestinal manifestations, and even colitis-associated cancer [2]. The etiology of IBD is associated with the genetics, gut microbiota, immune responses, and the environmental factors [3]. The aberrant immune responses are demonstrated to be closely associated with the chronic inflammation in IBD.
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