Abstract
Background
Atopic dermatitis (AD) is a chronic immune and inflammatory dermatologic disease. Preclinical and clinical studies have indicated that stem cell transplantation is considered an alternative treatment option for ameliorating the symptoms of AD. However, the molecular mechanisms by which stem cells treat AD remain unclear. This study aimed to evaluate the therapeutic effects of Wharton’s jelly mesenchymal stem cells in a 2,4-dinitrofluorobenzene (DNFB)-induced mouse model of AD.
Methods
Human Wharton’s jelly-mesenchymal stem cells (hWJ-MSCs) were subcutaneously injected into mice receiving DNFB on day 7 (DNFB-MSC 7 group) and days 7 and 16 (DNFB-MSC 7, 16 group).
Results
hWJ-MSCs improved the symptoms of AD and lowered the clinical skin score. After treatment with hWJ-MSCs, the skin thickness of the epidermis was reduced in AD mice. hWJ-MSCs decreased the serum concentration of IgE. Mechanically, hWJ-MSCs inhibited the expression of proteins associated with the NLRP3 inflammasome, such as NLRP3, ASC/TMS1, TXNIP, and caspase-1. Furthermore, hWJ-MSCs regulated the expression of TGF-β1 and histone deacetylase 3 (HDAC3) proteins.
Conclusions
Taking these results together, treatment with hWJ-MSCs improved the clinical symptoms by regulating TXNIP/NLRP3 and HDAC3/TGF-β1 signaling cascade.