Literature DB >> 8546480

Staphylococcal enterotoxin B applied on intact normal and intact atopic skin induces dermatitis.

P Strange1, L Skov, S Lisby, P L Nielsen, O Baadsgaard.   

Abstract

BACKGROUND AND
DESIGN: Colonization of inflammatory skin diseases with Staphylococcus aureus is a frequent phenomenon and may cause exacerbation of the skin disease. Staphylococcus aureus strains present on atopic dermatitis are capable of releasing staphylococcal enterotoxins, a group of superantigens that are very potent T-cell activators. To determine whether the superantigen staphylococcal enterotoxin B can induce inflammation when applied on the skin, staphylococcal enterotoxin B was applied with and without occlusion on the volar aspect of the skin on the forearm of 10 subjects without skin disease and six subjects with atopic dermatitis of minimal activity and no eczema on the volar aspect of the skin on their forearm. The main outcome measures were clinical rating; determination of the increase of the thickness of the skin-fold; and determination of skin blood flow.
RESULTS: Clinically, staphylococcal enterotoxin B induced skin changes of erythema and induration in 10 of 10 healthy volunteer subjects and six of six subjects suffering from atopic dermatitis, while the vehicle induced clinically evident skin changes in only one of 10 healthy subjects and none of six subjects with atopic dermatitis. On day 3 after the application of an occluded patch containing 10 micrograms/cm2 of staphylococcal enterotoxin B in the healthy subjects, the thickness of the skinfold increased 0.47 +/- 0.49 mm (mean +/- SD) (n = 9; P < .02) relative to the increase in the thickness of the skinfold following application of the vehicle. The Doppler laser-measured skin blood flow index had increased from 1.0 +/- 0.4 to 5.3 +/- 3.7 (mean +/- SD) (n = 10; P < .002). On day 3 after the application of occluded patchs containing 10 micrograms/cm2 of staphylococcal enterotoxin B in the subjects suffering from atopic dermatitis, the increase in the thickness of the skinfold increased 0.20 +/- 0.24 mm (n = 6; P, not significant) relative to the increased thickness in the skinfold following application of the vehicle. The Doppler laser-measured skin blood flow index had increased from 1.1 +/- 0.4 to 3.7 +/- 2.2 (n = 6, P, not significant). Three of six subjects suffering from atopic dermatitis experienced a flare of their disease in the elbow flexure ipsilaterally to where the staphylococcal enterotoxin B patch was applied.
CONCLUSIONS: The superantigen staphylococcal enterotoxin B applied on intact skin from both normal subjects and patients with atopic dermatitis induces an inflammatory reaction. This finding suggests that superantigens released from S aureus present on the skin in inflammatory skin diseases may exacerbate and sustain the inflammation.

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Year:  1996        PMID: 8546480

Source DB:  PubMed          Journal:  Arch Dermatol        ISSN: 0003-987X


  31 in total

1.  Epidermal HLA-DR and the enhancement of cutaneous reactivity to superantigenic toxins in psoriasis.

Authors:  J B Travers; Q A Hamid; D A Norris; C Kuhn; R C Giorno; P M Schlievert; E R Farmer; D Y Leung
Journal:  J Clin Invest       Date:  1999-11       Impact factor: 14.808

2.  T cells and effector mechanisms in the pathogenesis of atopic dermatitis.

Authors:  Mübeccel Akdis; Axel Trautmann; Kurt Blaser; Cezmi A Akdis
Journal:  Curr Allergy Asthma Rep       Date:  2002-01       Impact factor: 4.806

3.  Staphylococcal toxin-induced T cell proliferation in atopic eczema correlates with increased use of superantigen-reactive Vbeta-chains in cutaneous lymphocyte-associated antigen (CLA)-positive lymphocytes.

Authors:  S Davison; M Allen; R Vaughan; J Barker
Journal:  Clin Exp Immunol       Date:  2000-08       Impact factor: 4.330

Review 4.  Cutaneous perspectives on adaptive immunity.

Authors:  Michael Girardi
Journal:  Clin Rev Allergy Immunol       Date:  2007-10       Impact factor: 8.667

5.  Mutational analysis of superantigen activity responsible for the induction of skin erythema by streptococcal pyrogenic exotoxin C.

Authors:  J Yamaoka; E Nakamura; Y Takeda; S Imamura; N Minato
Journal:  Infect Immun       Date:  1998-10       Impact factor: 3.441

6.  Staphylococcus aureus Isolated from Skin from Atopic-Dermatitis Patients Produces Staphylococcal Enterotoxin Y, Which Predominantly Induces T-Cell Receptor Vα-Specific Expansion of T Cells.

Authors:  Fatkhanuddin Aziz; Junzo Hisatsune; Liansheng Yu; Junko Kajimura; Yusuke Sato'o; Hisaya K Ono; Kanako Masuda; Mika Yamaoka; Siti Isrina Oktavia Salasia; Akio Nakane; Hiroki Ohge; Yoichiro Kusunoki; Motoyuki Sugai
Journal:  Infect Immun       Date:  2020-01-22       Impact factor: 3.441

7.  Role of staphylococcal superantigen in atopic dermatitis: influence on keratinocytes.

Authors:  Kyu Han Kim; Ji Hyun Han; Jin Ho Chung; Kwang Hyun Cho; Hee Chul Eun
Journal:  J Korean Med Sci       Date:  2006-04       Impact factor: 2.153

Review 8.  Influences on allergic mechanisms through gut, lung, and skin microbiome exposures.

Authors:  Andrea M Kemter; Cathryn R Nagler
Journal:  J Clin Invest       Date:  2019-02-25       Impact factor: 14.808

Review 9.  Role of bacterial pathogens in atopic dermatitis.

Authors:  Yu-Tsan Lin; Chen-Ti Wang; Bor-Luen Chiang
Journal:  Clin Rev Allergy Immunol       Date:  2007-12       Impact factor: 8.667

Review 10.  The role of microorganisms in atopic dermatitis.

Authors:  Barbara S Baker
Journal:  Clin Exp Immunol       Date:  2006-04       Impact factor: 4.330

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