MyD88 Contributes to Staphylococcal Enterotoxin B-Triggered Atopic Dermatitis-Like Skin Inflammation in Mice

Faßbender, Sonja; Opitz, Friederike V.; Johnen, Sarah; Förster, Irmgard

doi:10.1016/j.jid.2017.04.015

Cited by 4 publications

(3 citation statements)

References 15 publications

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“…Some studies point out that alterations in the MyD88 pathway are needed for the development of a SEB-induced AD-like phenotype and it has been demonstrated that SEB increases the expression of TLR2, improving the host’s reaction to other microbial products. 12 , 29 …”

Section: Discussionmentioning

confidence: 99%

Increased Expression of Toll-Like Receptor (TLR) 2 and TLR6 on Peripheral Blood Monocytes by Induction of Staphylococcal Enterotoxin B During Exacerbation of Atopic Dermatitis Patients

Salim¹,

Gunawan²,

Suwarsa³

et al. 2023

CCID

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Background Atopic dermatitis (AD) is a chronic and recurrent inflammatory skin disease that can be triggered by various precipitating factors, including colonization by Staphylococcus aureus ( S. aureus ). The toll-like receptor (TLR), which belongs to the family of pattern recognition receptors (PRR), can recognize components of S. aureus , such as staphylococcal enterotoxin B (SEB). This receptor is known to be expressed on monocytes. However, the understanding of the role of SEB in the pathogenesis of AD through the TLR pathway, especially TLR2 and TLR6, is not widely known. Purpose To investigate the expression of TLR2 and TLR6 on peripheral blood monocytes induced by SEB during AD exacerbations. Patients and Methods Twenty AD patients and 20 healthy subjects as a control group were selected. A 5 mL blood sample from each subject was taken for monocyte culture, which was induced by SEB for three days, and the outcomes were assessed by flow cytometry to evaluate TLR2 and TLR6 expression. Results The expression of TLR2 on peripheral blood monocytes in AD patients was increased compared to healthy controls ( p = 0.000), but not for the expression of TLR6 ( p = 0.304). In the AD group, TLR2 and TLR6 expression on peripheral blood monocytes after being induced by SEB was significantly increased compared to before induction ( p = 0.025 and p = 0.023, respectively), but not in the control group ( p = 0.737 and p = 0.100, respectively). Conclusion There is significantly increased expression of TLR2 and TLR6 on peripheral blood monocytes induced by SEB during exacerbation in AD patients.

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Section: Discussionmentioning

confidence: 99%

Increased Expression of Toll-Like Receptor (TLR) 2 and TLR6 on Peripheral Blood Monocytes by Induction of Staphylococcal Enterotoxin B During Exacerbation of Atopic Dermatitis Patients

Salim¹,

Gunawan²,

Suwarsa³

et al. 2023

CCID

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“…The dysfunction in TLR response in AD patients can be associated with deficiencies in the signaling components. Some studies point out that alterations in the myeloid differentiation protein (MyD88) pathway is needed for the development of SEB-induced AD-like phenotype [20,21].…”

Section: Role Of S Aureus Toxins In the Disruption Of The Skin Bamentioning

confidence: 99%

Exploring the Role of Staphylococcus Aureus Toxins in Atopic Dermatitis

Yoshikawa

Lima

Sato

et al. 2019

Toxins

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Atopic dermatitis (AD) is a chronic and inflammatory skin disease with intense pruritus and xerosis. AD pathogenesis is multifactorial, involving genetic, environmental, and immunological factors, including the participation of Staphylococcus aureus. This bacterium colonizes up to 30–100% of AD skin and its virulence factors are responsible for its pathogenicity and antimicrobial survival. This is a concise review of S. aureus superantigen-activated signaling pathways, highlighting their involvement in AD pathogenesis, with an emphasis on skin barrier disruption, innate and adaptive immunity dysfunction, and microbiome alterations. A better understanding of the combined mechanisms of AD pathogenesis may enhance the development of future targeted therapies for this complex disease.

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“…Successful candidates may be selected for preclinical development including an appropriate formulation for either topical or systemic administration. Thereafter, the candidate can be further evaluated in more sophisticated animal models such as the ovalbumin‐induced dermatitis model in mice or the canine model of atopic dermatitis …”

Section: Repurposing Of Neuropharmacological Drugs For Inflammatory Smentioning

confidence: 99%

Can we teach old drugs new tricks?—Repurposing of neuropharmacological drugs for inflammatory skin diseases

Abels

Soeberdt

2019

Experimental Dermatology

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Despite the “hype” for monoclonal antibodies, the so‐called biologics, which added significant value to the therapeutic armamentarium of dermatologists and improved the life of many patients, but may exhibit significant adverse effects, the vast majority of dermatological patients suffering from atopic dermatitis or psoriasis is still treated topically. Thus, there is a huge need for locally applied, locally acting drugs for inflammatory skin diseases with better risk‐benefit profiles compared to topical corticosteroids or calcineurin inhibitors. Drug repositioning is a complex process, but offers advantages, in particular for indications with lower revenues. In this viewpoint, the neuroendocrine system of the skin is described as an attractive drug target because it contributes significantly to neutralizing external noxious agents prior to inducing immune or vascular changes leading to the clinical signs of skin inflammation, for example, itch and erythema. In addition, epidermis and dermis are accessible for topically applied products which may act locally without pharmacodynamically relevant systemic exposure limiting adverse events. Moreover, since numerous drugs have been evaluated for various CNS diseases, some failed and some approved, this resource should be exploited for repurposing as anti‐inflammatory drugs for topical application, for example, cannabidiol, fingolimod or asimadoline. Finally, a screening algorithm is shared which gives direct evidence of links between drug and inflammatory skin diseases.

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MyD88 Contributes to Staphylococcal Enterotoxin B-Triggered Atopic Dermatitis-Like Skin Inflammation in Mice

Abstract: B, et al. Human epithelial cells trigger dendritic cell mediated allergic inflammation by producing TSLP. Nat Immunol 2002;3:673e80.

Cited by 4 publications

References 15 publications

Increased Expression of Toll-Like Receptor (TLR) 2 and TLR6 on Peripheral Blood Monocytes by Induction of Staphylococcal Enterotoxin B During Exacerbation of Atopic Dermatitis Patients

Increased Expression of Toll-Like Receptor (TLR) 2 and TLR6 on Peripheral Blood Monocytes by Induction of Staphylococcal Enterotoxin B During Exacerbation of Atopic Dermatitis Patients

Exploring the Role of Staphylococcus Aureus Toxins in Atopic Dermatitis

Can we teach old drugs new tricks?—Repurposing of neuropharmacological drugs for inflammatory skin diseases

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