Staphylococcus aureus in atopic dermatitis: Strain-specific cell wall proteins and skin immunity

Iwamoto, Kazumasa; Moriwaki, Masaya; Miyake, Ryu

doi:10.1016/j.alit.2019.02.006

Cited by 79 publications

(81 citation statements)

References 63 publications

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“…96,97 The barrier-disrupted AD skin is susceptible to microbial colonization such as Staphylococcus aureus, which further promotes Th2-prone immune response. 98 Recent therapeutic success obtained by an anti-IL-4 receptor a chain (IL-4Ra) antibody, dupilumab, implicates a pivotal role for IL-4 and IL-13 in the pathogenesis of AD, as dupilumab interferes with both IL-4 and IL-13 signaling. 99 IL-4 and IL-13 activate signal transducer and activator of transcription 6 and then inhibit the expression of filaggrin, loricrin and involucrin.…”

Section: Ad and Scratch Injury Infiltration Of Th17/th22 Cells And Scmentioning

confidence: 99%

Pathogenic implication of epidermal scratch injury in psoriasis and atopic dermatitis

Furue

Ulzii

Tanaka

et al. 2020

The Journal of Dermatology

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Mechanical scratching, a common external stress affecting the skin, is induced by various causes, such as pruritus. Scratch injury to epidermal keratinocytes upregulates the production and release of chemokine (C‐C motif) ligand 20 (CCL20) in vitro, which selectively chemoattracts interleukin (IL)‐17A‐producing immune cells that express chemokine (C‐C motif) receptor 6 (CCR6). In IL‐17A‐dominant psoriasis, scratch‐induced CCL20 upregulation and subsequent accumulation of IL‐17A‐producing immune cells and CCR6+ mature dendritic cells may trigger the development of psoriatic lesions, a process known as the Koebner phenomenon. In IL‐4/IL‐13‐dominant atopic dermatitis, pruritus and subsequent scratching are the primary symptoms. Scratch‐induced CCL20 production from keratinocytes may explain why IL‐17A levels are also elevated in atopic dermatitis. In contrast, mechanical scratching is likely to negatively regulate IL‐13 signaling by upregulating the expression of IL‐13 receptor α2, which serves as a decoy receptor for IL‐13 in keratinocytes. In this review, we summarize current reports on topics related to the pathogenic role of epidermal scratch injury in psoriasis and atopic dermatitis.

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Section: Ad and Scratch Injury Infiltration Of Th17/th22 Cells And Scmentioning

confidence: 99%

Pathogenic implication of epidermal scratch injury in psoriasis and atopic dermatitis

Furue

Ulzii

Tanaka

et al. 2020

The Journal of Dermatology

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“…Aberrations of the immune system have long been considered as having key roles, until recently; molecular epidemiology has tended to focus on the skin microbiome as a common precursor and pathological feature. At present, the pathology of AD includes three critical factors: impaired skin barrier function, microbial dysbiosis, and cutaneous immune abnormality predisposed to T helper 2 (Th2) immunity, which may aggravate one another [19,20].…”

Section: Skin Microbiome Profiling In Patients With Admentioning

confidence: 99%

“…The result showed that clinical improvement is positively correlated with increased favorable microbial community and reduced abundance of S. aureus [46]. More novel systemic immunomodulatory agents for AD are under development, and it is promising that these therapies will not only improve skin immunity but also adjust S. aureus colonization by modulating their cell wall proteins [19].…”

Section: Biological Therapy In Patients With Admentioning

confidence: 99%

A Calm, Dispassionate Look at Skin Microbiota in Atopic Dermatitis: An Integrative Literature Review

Wan

Chen

2020

Dermatol Ther (Heidelb)

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Atopic dermatitis (AD) is a chronic common inflammatory skin disorder with clinical characteristics of pruritic, dry, and recurrent flares that involve the whole body. Recent studies have demonstrated that the skin microbiota, characterized by an overgrowth of Staphylococcus aureus (S. aureus), plays a critical role in the manifestation of AD. There is striking evidence that skin microbiota can modulate the development and progression of AD. Therefore, more and more therapeutic approaches are adopted for modifying skin microbiota. Here we discuss the role of skin microbiota in the etiology and maintenance of AD; furthermore, we summarize the effects of therapeutic treatments on skin microbiota in AD based on published literature. With the help of the theoretical guidance suggested by microbial metagenome analysis, the reconstitution of microbiota should be a promising way to harness the pathogens of AD and could be used as a brandnew therapeutic strategy in clinical trials. We believe that the targeted therapy of dysbiosis in AD may possibly become a unique approach to an integrated treatment program in the near future.

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“…CoNS are typically low virulence organisms that commonly colonize the skin and mucous membranes. CoNS, including S. epidermidis, compete with S. aureus for stable colonization of human skin reservoirs by production of antimicrobial factors [7,9,19].…”

Section: Discussionmentioning

confidence: 99%

“…Current treatments for AD with the usage of topical steroids improve dermatitis due to their strong anti-inflammatory effect. However, skin thinning with long-term use and recurrence of dermatitis after discontinuation are highly associated [9]. In order to compensate for these limitations in those conventional topical steroid treatments, several attempts have been made to achieve the removal of colonized S. aureus.…”

Section: Introductionmentioning

confidence: 99%

Novel Cytoplasmic Bacteriocin Compounds Derived from Staphylococcus epidermidis Selectively Kill Staphylococcus aureus, Including Methicillin-Resistant Staphylococcus aureus (MRSA)

et al. 2020

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Staphylococcus aureus (S. aureus) is one of the well-known agents causing atopic dermatitis (AD) in susceptible individuals, and Staphylococcus epidermidis (S. epidermidis) produces class I thermostable bacteriocins that can selectively kill S. aureus, suggesting protective roles against AD. There is a large need for developing precise therapies only to target S. aureus and not to harm the beneficial microbiome. On the agar well diffusion assay, live planktonic S. epidermidis showed clear zones of inhibition of S. aureus growth, but heat-killed cells and cell-free supernatants did not show this. These results would lead us to hypothesize that cytoplasmic bacteriocin from S. epidermidis will be a promising agent to inhibit S. aureus growth. Therefore, we have extracted a novel thermolabile cytoplasmic bacteriocin from S. epidermidis using trichloroactic acid (TCA)/acetone precipitation method after cell lysis with a SDS-containing buffer. These bacteriocin selectively exhibited antimicrobial activity against S. aureus and methicillin-resistance Staphylococcus aureus (MRSA), presenting no active actions against S. epidermidis, E. coli, and Salmonella Typhimurium. The extracted cytoplasmic bacteriocin compounds revealed several diffuse bands of approximately 40–70 kDa by SDS-PAGE. These findings suggest that these cytoplasmic bacteriocin compounds would be a great potential means for S. aureus growth inhibition and topical AD treatment.

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Staphylococcus aureus in atopic dermatitis: Strain-specific cell wall proteins and skin immunity

Cited by 79 publications

References 63 publications

Pathogenic implication of epidermal scratch injury in psoriasis and atopic dermatitis

Pathogenic implication of epidermal scratch injury in psoriasis and atopic dermatitis

A Calm, Dispassionate Look at Skin Microbiota in Atopic Dermatitis: An Integrative Literature Review

Novel Cytoplasmic Bacteriocin Compounds Derived from Staphylococcus epidermidis Selectively Kill Staphylococcus aureus, Including Methicillin-Resistant Staphylococcus aureus (MRSA)

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