Therapeutic Effect of EGF Secreted by Human Umbilical Cord Blood-Derived Mesenchymal Stem Cells on Atopic Dermatitis

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This study by Jung et al. investigates the therapeutic potential of epidermal growth factor (EGF) secreted by human umbilical cord blood-derived mesenchymal stem cells (hUCB-MSCs) in treating atopic dermatitis (AD). AD is a chronic inflammatory skin disorder marked by severe itching, dryness, and erythema. The study explores how EGF from hUCB-MSCs can modulate inflammatory responses in keratinocytes, Th2 cells, and mast cells, which are key players in AD pathology. The study demonstrated that hUCB-MSCs secrete high levels of EGF, which plays a crucial role in reducing AD symptoms by regulating the activity of these inflammatory cells. Using a Dermatophagoides farinae-induced AD mouse model, the research showed that EGF-depleted hUCB-MSCs had significantly attenuated therapeutic effects compared to untreated hUCB-MSCs, confirming the importance of EGF in ameliorating AD symptoms.

Atopic dermatitis (AD) is a prevalent chronic inflammatory skin disease that often begins in early childhood and can persist into adulthood. It is characterized by intense itching, dry skin, and inflamed lesions, severely affecting patients' quality of life. Traditional treatments for AD, such as topical steroids and immunosuppressants, often provide limited relief and can have significant side effects. Recent advances in stem cell therapy, particularly using mesenchymal stem cells (MSCs), offer new therapeutic possibilities for managing AD.

This study by Jung et al. focuses on the role of epidermal growth factor (EGF) secreted by human umbilical cord blood-derived MSCs (hUCB-MSCs) in treating AD. MSCs are known for their immunomodulatory properties and ability to secrete various growth factors that aid in tissue repair and inflammation reduction. The research aimed to understand how EGF from hUCB-MSCs influences the inflammatory environment in AD.

The researchers first confirmed that hUCB-MSCs secrete significantly higher levels of EGF compared to other cell types. They used small interfering RNA (siRNA) to downregulate EGF expression in hUCB-MSCs and then co-cultured these cells with keratinocytes, Th2 cells, and mast cells to assess the impact on AD-related inflammation. The depletion of EGF disrupted the immunomodulatory effects of hUCB-MSCs on these cells, leading to increased inflammation and mast cell degranulation.

In an in vivo model, AD was induced in NC/Nga mice using Dermatophagoides farinae extract. The mice were then treated with subcutaneous injections of either untreated or EGF-depleted hUCB-MSCs. The results showed that mice treated with EGF-depleted hUCB-MSCs had higher levels of inflammatory cytokines (IL-4, TNF-α, TARC, IL-22) and serum IgE, increased mast cell infiltration, and worsened clinical symptoms compared to those treated with untreated hUCB-MSCs. Histopathological analysis revealed that EGF depletion significantly impaired the ability of hUCB-MSCs to reduce epidermal and ear thickness and to decrease mast cell infiltration in skin lesions.

These findings highlight the crucial role of EGF secreted by hUCB-MSCs in modulating the immune response and promoting skin healing in AD. EGF was shown to inhibit the expression of pro-inflammatory cytokines and the degranulation of mast cells, thereby alleviating the symptoms of AD. The study suggests that enhancing EGF secretion by hUCB-MSCs could be a viable strategy to improve the efficacy of stem cell therapy for AD and potentially other inflammatory skin diseases.

The therapeutic effects of EGF secreted by hUCB-MSCs, as demonstrated in this study, are closely aligned with the objectives of Novastem's stem cell therapies, which aim to regenerate and repair damaged tissues. The ability of hUCB-MSCs to modulate immune responses and promote tissue repair suggests that Novastem's treatments could offer similar benefits for conditions characterized by chronic inflammation and immune dysregulation, such as atopic dermatitis and other inflammatory skin diseases.

  • Mechanism of Action: EGF secreted by hUCB-MSCs modulates immune responses by inhibiting the activity of Th2 cells, B cells, and mast cells, and promoting keratinocyte regeneration.
  • Clinical Benefits: The administration of hUCB-MSCs significantly reduces AD symptoms, including inflammation and mast cell infiltration, by secreting EGF, which plays a crucial role in the therapeutic process.
  • Potential for Broad Application: The success of EGF-secreting hUCB-MSCs in treating AD suggests their potential applicability to other inflammatory and immune-mediated conditions, enhancing the scope of stem cell-based therapies.

#AtopicDermatitis #MesenchymalStemCells #EpidermalGrowthFactor #Immunomodulation #MastCellDegranulation #SkinInflammation #StemCellTherapy

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