Oral Administration of Heat-Killed Lactobacillus brevis SBC8803 Ameliorates the Development of Dermatitis and Inhibits Immunoglobulin E Production in Atopic Dermatitis Model NC/Nga Mice

Fungi including Malassezia furfur and Candida albicans are involved in the development of atopic dermatitis (AD), due to increased sensitivity to these allergens or increased serum immunoglobulin E levels in AD patients. Previously, I reported successful treatment of AD with oral administration of the anti-mycotic agent, itraconazole. Recently, I developed protocols for AD treatment, based on the determined minimum effective dose. Three oral administration regimens with itraconazole were studied: single-phase treatment (regimen 1), 100 mg/day for 1 week with a 3-week rest, repeating; regimen 2, 200 mg/week for 4 weeks, repeating; and dual-phase treatment (regimen 3), 100 mg/day for 1 week (introduction phase) then 200 mg/week (maintenance phase) for 11 weeks. For regimens 1 and 2, each treatment cycle was 4 weeks, and three cycles were undertaken. Each regimen was completed in 12 weeks. All three regimens reduced AD symptoms, regimen 3 being the most effective and efficient therapy as evaluated by overall efficacy and low drop-out rate.

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Immunoglobulin E in dermatoses. Levels in atopic dermatitis and urticaria

Archives of Dermatology ◽

10.1001/archderm.100.1.12 ◽

1969 ◽

Vol 100 (1) ◽

pp. 12-16 ◽

Cited By ~ 98

Author(s):

L. Juhlin

Keyword(s):

Atopic Dermatitis ◽

Immunoglobulin E

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Effects of mineral complex material treatment on 2,4- dinitrochlorobenzene-induced atopic dermatitis like-skin lesions in mice model

BMC Complementary Medicine and Therapies ◽

10.1186/s12906-021-03259-5 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Johny Bajgai ◽

Jing Xingyu ◽

Ailyn Fadriquela ◽

Rahima Begum ◽

Dong Heui Kim ◽

...

Keyword(s):

Atopic Dermatitis ◽

Water Loss ◽

Immunoglobulin E ◽

Skin Barrier ◽

Skin Lesions ◽

Total Serum ◽

Skin Barrier Function ◽

Barrier Dysfunction ◽

Complex Material ◽

Mineral Complex

Abstract Background Atopic dermatitis (AD) is a chronic allergic inflammatory skin disease characterized by complex pathogenesis including skin barrier dysfunction, immune-redox disturbances, and pruritus. Prolonged topical treatment with medications such as corticosteroids, calcineurin inhibitors, and T-cell inhibitors may have some potential side-effects. To this end, many researchers have explored numerous alternative therapies using natural products and mineral compounds with antioxidant or immunomodulatory effects to minimize toxicity and adverse-effects. In the current study, we investigated the effects of mineral complex material (MCM) treatment on 2, 4-dinitrochlorobenzene (DNCB)-induced AD-like skin lesions in SKH-1 hairless mice. Methods Animals were divided into four groups; normal control (NC), negative control treated with DNCB only (DNCB only), positive control treated with DNCB and tacrolimus ointment (PC) and experimental group treated with DNCB and MCM patch (MCM). Skin inflammation and lesion severity were investigated through analyses of skin parameters (barrier score and strength, moisture and trans-epidermal water loss level), histopathology, immunoglobulin E, and cytokines. In addition, reactive oxygen species (ROS), nitric oxide (NO), glutathione peroxidase (GPx), and catalase (CAT) levels were measured in both serum and skin lysate. Results Our results demonstrates that MCM patch improved the progression of AD-like skin lesions by significantly increasing skin barrier strength and decreasing trans-epidermal water loss. Additionally, dermal administration of MCM patch significantly reduced epidermal thickness, ROS, and NO levels in skin lysate. Furthermore, we found that MCM suppressed the levels of AD-involved (Th1 and Th2) cytokines such as IL-2, IFN-γ, and IL-4 in blood. In addition, the levels of other Th1, and Th2 and inflammatory cytokines such as IL-1β, TNF-α, IL-6, IL-12(p70) and IL-10 were found lowest in the MCM group than in the DNCB only and PC groups. Moreover, we found total serum IgE level significantly increased after DNCB treatment, but decreased in the PC and MCM groups. Conclusion Taken together, our findings suggest that MCM application may have beneficial effects either systemic or regional on DNCB-induced AD lesional skin via regulation of the skin barrier function and immune-redox response.

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Analysis of pediatric atopic dermatitis: The relationship between disease progression and total immunoglobulin E and percent positive immunocaps

Journal of the American Academy of Dermatology ◽

10.1016/j.jaad.2012.12.705 ◽

2013 ◽

Vol 68 (4) ◽

pp. AB170

Keyword(s):

Atopic Dermatitis ◽

Disease Progression ◽

Immunoglobulin E ◽

The Relationship ◽

Total Immunoglobulin

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Gomisin M2 Ameliorates Atopic Dermatitis-like Skin Lesions via Inhibition of STAT1 and NF-κB Activation in 2,4-Dinitrochlorobenzene/Dermatophagoides farinae Extract-Induced BALB/c Mice

Molecules ◽

10.3390/molecules26154409 ◽

2021 ◽

Vol 26 (15) ◽

pp. 4409

Author(s):

Jinjoo Kang ◽

Soyoung Lee ◽

Namkyung Kim ◽

Hima Dhakal ◽

Taeg-Kyu Kwon ◽

...

Keyword(s):

Atopic Dermatitis ◽

Oral Administration ◽

Skin Diseases ◽

Nuclear Translocation ◽

Skin Lesions ◽

Biologically Active ◽

Therapeutic Effects ◽

Dermatophagoides Farinae ◽

Tnf Α ◽

Ifn Γ

The extracts of Schisandra chinensis (Turcz.) Baill. (Schisandraceae) have various therapeutic effects, including inflammation and allergy. In this study, gomisin M2 (GM2) was isolated from S. chinensis and its beneficial effects were assessed against atopic dermatitis (AD). We evaluated the therapeutic effects of GM2 on 2,4-dinitrochlorobenzene (DNCB) and Dermatophagoides farinae extract (DFE)-induced AD-like skin lesions with BALB/c mice ears and within the tumor necrosis factor (TNF)-α and interferon (IFN)-γ-stimulated keratinocytes. The oral administration of GM2 resulted in reduced epidermal and dermal thickness, infiltration of tissue eosinophils, mast cells, and helper T cells in AD-like lesions. GM2 suppressed the expression of IL-1β, IL-4, IL-5, IL-6, IL-12a, and TSLP in ear tissue and the expression of IFN-γ, IL-4, and IL-17A in auricular lymph nodes. GM2 also inhibited STAT1 and NF-κB phosphorylation in DNCB/DFE-induced AD-like lesions. The oral administration of GM2 reduced levels of IgE (DFE-specific and total) and IgG2a in the mice sera, as well as protein levels of IL-4, IL-6, and TSLP in ear tissues. In TNF-α/IFN-γ-stimulated keratinocytes, GM2 significantly inhibited IL-1β, IL-6, CXCL8, and CCL22 through the suppression of STAT1 phosphorylation and the nuclear translocation of NF-κB. Taken together, these results indicate that GM2 is a biologically active compound that exhibits inhibitory effects on skin inflammation and suggests that GM2 might serve as a remedy in inflammatory skin diseases, specifically on AD.

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Ubiquitous Overexpression of Chromatin Remodeling Factor SRG3 Exacerbates Atopic Dermatitis in NC/Nga Mice by Enhancing Th2 Immune Responses

International Journal of Molecular Sciences ◽

10.3390/ijms22041553 ◽

2021 ◽

Vol 22 (4) ◽

pp. 1553

Author(s):

Sung Won Lee ◽

Hyun Jung Park ◽

Jungmin Jeon ◽

Yun Hoo Park ◽

Tae-Cheol Kim ◽

...

Keyword(s):

Atopic Dermatitis ◽

Mast Cells ◽

Immune Responses ◽

Chromatin Remodeling ◽

Skin Diseases ◽

Immunoglobulin E ◽

Critical Role ◽

Interleukin 4 ◽

Inflammatory Skin Diseases ◽

Immune Disorder

The SWItch (SWI)3-related gene (SRG3) product, a SWI/Sucrose Non-Fermenting (SNF) chromatin remodeling subunit, plays a critical role in regulating immune responses. We have previously shown that ubiquitous SRG3 overexpression attenuates the progression of Th1/Th17-mediated experimental autoimmune encephalomyelitis. However, it is unclear whether SRG3 overexpression can affect the pathogenesis of inflammatory skin diseases such as atopic dermatitis (AD), a Th2-type immune disorder. Thus, to elucidate the effects of SRG3 overexpression in AD development, we bred NC/Nga (NC) mice with transgenic mice where SRG3 expression is driven by the β-actin promoter (SRG3β-actin mice). We found that SRG3β-actin NC mice exhibit increased AD development (e.g., a higher clinical score, immunoglobulin E (IgE) hyperproduction, and an increased number of infiltrated mast cells and basophils in skin lesions) compared with wild-type NC mice. Moreover, the severity of AD pathogenesis in SRG3β-actin NC mice correlated with expansion of interleukin 4 (IL4)-producing basophils and mast cells, and M2 macrophages. Furthermore, this accelerated AD development is strongly associated with Treg cell suppression. Collectively, our results have identified that modulation of SRG3 function can be applied as one of the options to control AD pathogenesis.

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