Staphylococcus aureus and atopic dermatitis

Dahl, Mark V.

doi:10.1001/archderm.119.10.840

Cited by 34 publications

(7 citation statements)

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“…4(C and D)) [8], suggesting that epidermal cells from those patients show abnormal production of the hitherto undiscovered epidermal enzyme termed SM deacylase. To exclude the possibility that the SM deacylase activity observed was due to contamination by bacteria, such as S. aureus, which are often present on the surface of the stratum corneum of AD patients [29,30], we examined whether high levels of SM deacylase activity were present in epidermis freed of bacteria by excessive tapestripping of the stratum corneum before biopsy. The SM deacylase activities of such tape-stripped skin was still higher than in AD patients [8], suggesting that the high SM deacylase activity noted is not derived from bacterial contamination of the stratum corneum.…”

Section: Sm Deacylase Activity In Admentioning

confidence: 99%

A possible mechanism underlying the ceramide deficiency in atopic dermatitis: Expression of a deacylase enzyme that cleaves the N-acyl linkage of sphingomyelin and glucosylceramide

Imokawa

2009

Journal of Dermatological Science

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Section: Sm Deacylase Activity In Admentioning

confidence: 99%

A possible mechanism underlying the ceramide deficiency in atopic dermatitis: Expression of a deacylase enzyme that cleaves the N-acyl linkage of sphingomyelin and glucosylceramide

Imokawa

2009

Journal of Dermatological Science

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“…The lipid layer of the skin also contributes to host defense mechanisms. It consists of oleic, searic and palmic acids that have potent antimicrobial activities [98, 99, 100]. Enhanced adherance of S. aureus to the skin of AD patients has been reported [98].…”

Section: Role Of Staphylococcus Aureus In the Pathogenesis Of Admentioning

confidence: 99%

Role of T Cells in Atopic Dermatitis

Herz¹,

Bunikowski

Renz³

1998

Int Arch Allergy Immunol

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Atopic dermatitis (AD) is a chronically relapsing inflammatory skin disease. Influx of activated T cells into the skin lesions represents a hallmark in AD. Recent results indicate a dynamic T-cell-derived cytokine production in AD. In addition to the well-known TH-2 component, chronic lesions and late-phase allergic responses are characterized by an TH-1/TH-0 cytokine pattern. Although there is no doubt that aeroallergens can contribute to the elicitation of acute- and late-phase allergic responses in AD, their role in the immunopathogenesis is controversally discussed. Recent attention has been given to the long-known phenomenon of persistent colonization of AD skin with S. aureus and the potential role of S. aureus-derived superantigens. Evidence from several in vitro and in vivo studies suggests that such bacterial superantigens have the potency to trigger chronic T-cell-mediated skin inflammation. Although these data are certainly suggestive, further clinical studies are required to elucidate the role of bacterial superantigens in initiation, maintenance and, especially, chronicity of skin inflammation.

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“…Microbial agents, such as Staphylococcus aureus, Pityrosporum yeast, Candida, and Trichophyton dermatophytes, act in two different ways to cause atopic dermatitis. The microorganisms directly invade the skin, creating local injury and inflammation, and induce a systemic allergic response to specific antigens, causing a rise in serum IgE and enhanced activity of the immune system [27,28]. The therapeutic use of heparin spray in two immunosuppressed patients (a child and a young person) with perineal dermatitis provided analgesic and anti-inflammatory effects.…”

Section: Discussionmentioning

confidence: 99%