Published online Dec 26, 2020. doi: 10.4252/wjsc.v12.i12.1623
Peer-review started: May 31, 2020
First decision: August 22, 2020
Revised: September 20, 2020
Accepted: October 12, 2020
Article in press: October 12, 2020
Published online: December 26, 2020
Processing time: 210 Days and 1.6 Hours
Autoimmune hepatitis (AIH) is a serious autoimmune liver disease that threatens human health globally, thus emphasizing the need to identify novel treatments. Stem cells from human exfoliated deciduous teeth (SHED), which are easy to non-invasively obtain, showed pronounced proliferative and immunomodulatory capacities.
AIH treatment requires long-term or even lifelong use of immunosuppressants, which may cause serious side effects. Some patients are insensitive to treatment and cannot be well controlled. More appropriate and effective medical technologies to cure diabetes are needed. Mesenchymal stem cell infusion could alleviate a variety of diseases such as AIH. SHED show more pronounced proliferative and im-munomodulatory capacities compared to bone marrow mesenchymal stem cells, and can differentiate into hepatocytes in vitro. Non-traumatically collected stem cells (SHED) may therefore be a promising option for treating AIH.
To investigate the protective effects of SHED on concanavalin A (ConA)-induced hepatitis in mice, and to elucidate the associated regulatory mechanisms.
We used a ConA-induced acute hepatitis mouse model (6–week-old to 8-week-old male Balb/c mice) and an in vitro co-culture system to study the protective effects of SHED on ConA-induced AIH, as well as the underlying mechanisms. Protocols were approved by the Animal Care and Use Committee of the Health Science Center, Peking University (No. 2015-186).
SHED infusion could prevent aberrant histopathological liver architecture caused by ConA-induced infiltration of CD3+, CD4+, tumor necrosis-alpha+, and interferon-gamma+ inflammatory cells. Alanine aminotransferase and aspartate aminotransferase were significantly elevated in hepatitis mice. SHED infusion could block the ConA-induced elevation of alanine aminotransferase and aspartate aminotransferase. Mechanistically, ConA upregulated tumor necrosis-alpha and interferon-gamma expression, which were activated by the nuclear factor-kappa B pathway, to induce hepatocyte apoptosis, resulting in acute liver injury. SHED administration protected hepatocytes from ConA-induced apoptosis.
We demonstrate that SHED exhibits protective effects in a ConA-induced AIH mouse model. SHED treatment could inhibit the activation of Th1 cells, and reduce the secretion of tumor necrosis-alpha and interferon-gamma expression to inhibit ConA-induced nuclear factor-kappa B pathway activation. This reduces both hepatocyte apoptosis and inflammatory liver damage.
These results could provide a potential prevention and therapeutic strategy for hepatitis and acute hepatic injury.