Published online Jul 14, 2020. doi: 10.3748/wjg.v26.i26.3750
Peer-review started: December 27, 2019
First decision: February 14, 2020
Revised: May 14, 2020
Accepted: June 3, 2020
Article in press: June 3, 2020
Published online: July 14, 2020
Processing time: 200 Days and 9.5 Hours
Crohn’s disease (CD) is a chronic relapsing inflammatory disorder of the gastrointestinal tract, especially involving the distal small intestine and the colonic mucosa. Conventional treatments are supportive rather than curative and have serious side effects.
Adipose-derived mesenchymal stem cells (ADSCs) have been gradually applied to treat various diseases. The therapeutic effect and underlying mechanism of ADSCs on CD are still not clear.
This study aimed to investigate the effect of ADSC administration on CD and explore potential mechanisms on intestinal epithelial cell regeneration, Wnt signaling, and T cell immunity.
Wistar rats were administered with 2,4,6-trinitrobenzene sulfonic acid (TNBS) to establish a rat model of CD, followed by tail injections of green fluorescent protein (GFP)-modified ADSCs. After tracing in vivo ADSC distribution, flow cytometry, qRT-PCR, and Western blot were used to detect changes in the Wnt signaling pathway, T cell subtypes, and their related cytokines.
The isolated cells showed the characteristics of ADSCs, including spindle-shaped morphology, high expression of CD29, CD44, and CD90, low expression of CD34 and CD45, and osteogenic/adipogenic ability. ADSC therapy markedly reduced disease activity index and ameliorated colitis severity in the TNBS-induced rat model of CD. Furthermore, serum anti-sacchromyces cerevisiae antibody and p-anti-neutrophil cytoplasmic antibody levels were significantly reduced in ADSC-treated rats. Mechanistically, the GFP-ADSCs were colocalized with intestinal epithelial cells in the CD rat model. GFP-ADSC delivery significantly antagonized TNBS-induced increased canonical Wnt pathway expression, decreased noncanonical Wnt signaling pathway expression, and increased apoptosis rates and protein level of cleaved caspase-3 in rats. In addition, ADSCs attenuated TNBS-induced abnormal inflammatory cytokine production, disturbed T cell subtypes, and their related markers in rats.
Successfully isolated ADSCs show co-location with IEC and therapeutic effects in CD by regulating IEC proliferation, the Wnt signaling pathway, and T cell immunity.
Systemic ADSC infusion may be a potential choice for CD therapy.