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Murine Colitis Modeling using Dextran Sulfate Sodium DSS
Published on: January 19, 2010
Exosomes released by granulocytic myeloid-derived suppressor cells attenuate DSS-induced colitis in mice
Yungang Wang1,2, Jie Tian2, Xinyi Tang1
1Department of Laboratory Medicine, The Affiliated People's Hospital, Jiangsu University, Zhenjiang, China.
Abstract:
Myeloid-derived suppressor cells (MDSC) have been described in inflammatory bowel disease (IBD), but their role in the disease remains controversial. We sought to define the effect of granulocytic MDSC-derived exosomes (G-MDSC exo) in dextran sulphate sodium (DSS)-induced murine colitis. G-MDSC exo-treated mice showed greater resistance to colitis, as reflected by lower disease activity index, decreased inflammatory cell infiltration damage. There was a decrease in the proportion of Th1 cells and an increase in the proportion of regulatory T cells (Tregs) in mesenteric lymph nodes (MLNs) from G-MDSC exo-treated colitis mice. Moreover, lower serum levels of interferon (IFN)-γ and tumor necrosis factor (TNF)-α were detected in G-MDSC exo-treated colitis mice. Interestingly, inhibition of arginase (Arg)-1 activity in G-MDSC exo partially abrogated the spontaneous improvement of colitis. In addition, G-MDSC exo could suppress CD4+ T cell proliferation and IFN-γ secretion in vitro and inhibit the delayed-type hypersensitivity (DTH) response, and these abilities were associated with Arg-1 activity. Moreover, G-MDSC exo promoted the expansion of Tregs in vitro. Taken together, these results suggest that G-MDSC exo attenuate DSS-induced colitis through inhibiting Th1 cells proliferation and promoting Tregs expansion.
Insights
Granulocytic myeloid-derived suppressor cell exosomes (G-MDSC exo) show therapeutic potential in inflammatory bowel disease (IBD). These exosomes reduce colitis severity by modulating immune cell populations and decreasing inflammatory markers.
Area of Science:
- Immunology
- Gastroenterology
Background:
- Myeloid-derived suppressor cells (MDSC) role in inflammatory bowel disease (IBD) is debated.
- Exosomes derived from granulocytic MDSC (G-MDSC exo) may influence IBD pathogenesis.
Purpose of the Study:
- To investigate the therapeutic effect of G-MDSC exo in dextran sulphate sodium (DSS)-induced murine colitis.
- To elucidate the underlying mechanisms of G-MDSC exo in modulating immune responses.
Main Methods:
- Induction of colitis in mice using DSS.
- Administration of G-MDSC exo to colitis models.
- Analysis of disease activity, inflammatory cell infiltration, and immune cell populations (Th1, Tregs) in mesenteric lymph nodes (MLNs).
- Measurement of serum inflammatory cytokines (IFN-γ, TNF-α).
- In vitro assays assessing G-MDSC exo's effects on CD4+ T cell proliferation, IFN-γ secretion, and Treg expansion, with and without arginase (Arg)-1 inhibition.
- Evaluation of the delayed-type hypersensitivity (DTH) response.
Main Results:
- G-MDSC exo treatment reduced colitis severity, indicated by lower disease activity index and less inflammatory cell infiltration.
- Treatment led to a decreased proportion of Th1 cells and an increased proportion of regulatory T cells (Tregs) in MLNs.
- Serum levels of IFN-γ and TNF-α were reduced in G-MDSC exo-treated mice.
- Inhibition of Arg-1 activity partially reversed the therapeutic benefits of G-MDSC exo.
- In vitro, G-MDSC exo suppressed CD4+ T cell proliferation and IFN-γ secretion, promoted Treg expansion, and these effects were linked to Arg-1 activity.
- G-MDSC exo inhibited the DTH response.
Conclusions:
- G-MDSC exo demonstrate a protective effect against DSS-induced colitis in mice.
- The therapeutic mechanism involves the inhibition of Th1 cell proliferation and promotion of Tregs expansion, partly mediated by Arg-1 activity.
- G-MDSC exo represent a potential cell-free therapeutic strategy for IBD.
