Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin disorder with a complex etiology involving the immune response. Recent studies have demonstrated the role of certain probiotics in the treatment and prevention of AD. However, the mechanism by which these probiotics regulate the immune system remains unclear. In this study, we examined the immunomodulatory capacity of Duolac ATP, a mixed formulation of probiotics, both in vitro and in vivo. Results showed that the expression of programmed death-ligand 1(PD-L1) was significantly upregulated on bone marrow-derived dendritic cells (BMDCs) treated with Duolac ATP. Furthermore, the anti-inflammatory cytokines IL-10 and TGF-beta were both upregulated when BMDCs were treated with Duolac ATP. The percentage of proliferated regulatory T cells (Tregs) was enhanced when CD4+ T cells were co-cultured with Duolac ATP-treated BMDCs on plates coated with anti-CD3/CD28 antibodies. Intriguingly, IL-10 secretion from CD4+ T cells was also observed. The AD symptoms, histologic scores, and serum IgE levels in AD mice were significantly decreased after oral treatment with Duolac ATP. Moreover, the Th1-mediated response in AD-induced mice treated with oral Duolac ATP showed upregulation of IL-2 and IFN-gamma as well as of downstream signaling molecules T-bet, STAT-1, and STAT-4. Conversely, Duolac ATP suppressed Th2 and Th17 responses in AD-like mice, as evidenced by the downregulation of GATA-3, C-maf, IL-4, IL-5, and IL-17. Additionally, Duolac ATP increased the number of Tregs found at Peyer’s patches (PP) in treated AD mice. These results suggest that Duolac ATP modulates DCs to initiate both Th1 and Treg responses in AD mice. Thus, Duolac ATP represents a potential preventative agent against AD and could serve as an effective immunomodulator in AD patients.

Highlights

  • Atopic dermatitis (AD) is a chronic inflammatory skin disorder that affects the structural and barrier functions of the skin

  • The aim of our study was to evaluate the efficacy of Duolac ATP within innate immune systems via bone marrow-derived dendritic cells (BMDCs) and to use a transcription factor and cytokine analysis of atopic mice to explore the mechanism by which Duolac ATP overcomes AD

  • BMDCs treated with Duolac ATP showed similar surface expressions of the co-stimulatory molecules CD86 and MHC II compared with untreated cells within the same intensity (Figure 1A) and percentage of cells (Figure 1B and Supplementary Figure S3)

Read more

Summary

Introduction

Atopic dermatitis (AD) is a chronic inflammatory skin disorder that affects the structural and barrier functions of the skin. Major symptoms of AD include excessive pruritus and eczema. The exact pathophysiology of AD is not yet fully understood, it can be caused by a combination of genetic, environmental, allergic, and microbial factors (Abramovits, 2005). AD is caused by an immune response – primarily T-helper (Th) 2 cell hypersensitivity. A balance between Th1 and Th2 cells is important for disease induction and tolerance. Steroid drugs are effective therapies, they have serious side effects, including dermal atrophy, acne, cataracts, growth retardation, and skin irritation. Long-term steroid treatment should generally be avoided (Gupta and Chow, 2003; Hengge et al, 2006). Other alternative therapeutic agents are being investigated, including herbs, phytochemicals, vitamins, and probiotics (Mainardi et al, 2009)

Objectives
Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call