Role of Bacterial Pathogens in Atopic Dermatitis

Lin, Yu-Tsan; Wang, Chen-Ti; Chiang, Bor‐Luen

doi:10.1007/s12016-007-0044-5

Cited by 86 publications

(85 citation statements)

References 146 publications

(237 reference statements)

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“…According to the present state knowledge, S. aureus colonisation reaches 75 -100% in lesional skin of AD patients, and 30 -100% of AD patients have this bacteria in their nonlesional skin. By contrast, only 5 -30% of healthy people are carriers of S. aureus [5,14,15,16,17]. The results of this study were consistent with thethe above observations -S. aureus was isolated from the skin lesions of 81% of AD patients.…”

Section: Discussionsupporting

confidence: 92%

“…It is widely known that inflammation in the course of AD is stimulated by the antigens of skin-colonising microorganisms. Damage to the epidermal barrier facilitates their penetration into the epidermis and dermis [5]. Staphylococcus aureus (S. aureus) has a predominant role among the pathogens responsible for exacerbation of the dermatological condition in AD patients [6,7].…”

Section: Introductionmentioning

confidence: 99%

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Skin and nasal vestibule colonisation by Staphylococcus aureus and its susceptibility to drugs in atopic dermatitis patients

Wróbel¹,

Tomczak²,

Jenerowicz³

et al. 2018

Ann Agric Environ Med.

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Introduction. Atopic dermatitis (AD) is a chronic and recurrent disease with an inflammatory background. Genetic and environmental factors are responsible for the occurrence and development of this dermatosis. Objective. The aim of the study was to assess the frequency of colonisation of the nasal vestibule and apparently healthy skin by S. aureus, and to assess dermal lesions for superinfection with S. aureus in AD patients. Materials and method. The research was performed on a population of 100 AD patients. Three smears were collected for microbiological investigations: from the anterior nares, from apparently healthy skin and from lesioned skin. On collection, the material was cultured on mediums provided by the bioMerieux and Argenta companies. The strains were identified and their sensitivity to antibiotics assessed by means of the Vitek2 system (bioMerieux). Results. S. aureus was present in at least one location in 90%. 44% presented S. aureus colonization of apparently healthy skin and within skin lesions. In the case of 23%, this particular pathogen was detected only in skin lesions, whereas 6% had a positive result within the area of apparently healthy skin. In total, S. aureus was detected in the skin of 73%. In 61%, apparently healthy skin had been colonized with S. aureus, whereas in 81% colonization was proved within the skin lesions. S. aureus was detected in the nasal vestibule of 85%. Among the group with S. aureus in their anterior nares, the pathogen was also found on the skin surface of 77%. Conclusions. S. aureus colonises skin in most AD patients. Most AD patients carry S. aureus in their nasal vestibules. S. aureus does not seem to colonise healthy skin as often as skin lesions in young people. The vast majority of S. aureus strains were sensitive to local antibiotics. Most S. aureus strains produced penicillinase.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Skin and nasal vestibule colonisation by Staphylococcus aureus and its susceptibility to drugs in atopic dermatitis patients

Wróbel¹,

Tomczak²,

Jenerowicz³

et al. 2018

Ann Agric Environ Med.

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“…S. aureus may also show enhanced adherence properties to skin cells, which has been shown when comparing atopic eczema sufferers with normal control subjects. 240,241 Other studies reviewed elsewhere 242,243 have suggested that the balance of pathogenic and synbiotic bacterial species on the skin is altered in atopic eczema, resulting in an agitated skin microbiome.…”

Section: Rationalementioning

confidence: 99%

Scoping systematic review of treatments for eczema

Nankervis

Kim

Delamere

et al. 2016

Programme Grants Appl Res

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BackgroundEczema is a very common chronic inflammatory skin condition.ObjectivesTo update the National Institute for Health Research (NIHR) Health Technology Assessment (HTA) systematic review of treatments for atopic eczema, published in 2000, and to inform health-care professionals, commissioners and patients about key treatment developments and research gaps.Data sourcesElectronic databases including MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials, Cochrane Skin Group Specialised Register, Latin American and Caribbean Health Sciences Literature (LILACS), Allied and Complementary Medicine Database (AMED) and Cumulative Index to Nursing and Allied Health Literature (CINAHL) were searched from the end of 2000 to 31 August 2013. Retrieved articles were used to identify further randomised controlled trials (RCTs).Review methodsStudies were filtered according to inclusion criteria and agreed by consensus in cases of uncertainty. Abstracts were excluded and non-English-language papers were screened by international colleagues and data were extracted. Only RCTs of treatments for eczema were included, as other forms of evidence are associated with higher risks of bias. Inclusion criteria for studies included availability of data relevant to the therapeutic management of eczema; mention of randomisation; comparison of two or more treatments; and prospective data collection. Participants of all ages were included. Eczema diagnosis was determined by a clinician or according to published diagnostic criteria. The risk of bias was assessed using the Cochrane Collaboration risk-of-bias tool. We used a standardised approach to summarising the data and the assessment of risk of bias and we made a clear distinction between what the studies found and our own interpretation of study findings.ResultsOf 7198 references screened, 287 new trials were identified spanning 92 treatments. Trial reporting was generally poor (randomisation method: 2% high, 36% low, 62% unclear risk of bias; allocation concealment: 3% high, 15% low, 82% unclear risk of bias; blinding of the intervention: 15% high, 28% low, 57% unclear risk of bias). Only 22 (8%) trials were considered to be at low risk of bias for all three criteria. There was reasonable evidence of benefit for the topical medications tacrolimus, pimecrolimus and various corticosteroids (with tacrolimus superior to pimecrolimus and corticosteroids) for both treatment and flare prevention; oral ciclosporin; oral azathioprine; narrow band ultraviolet B (UVB) light; Atopiclair™ and education. There was reasonable evidence to suggest no clinically useful benefit for twice-daily compared with once-daily topical corticosteroids; corticosteroids containing antibiotics for non-infected eczema; probiotics; evening primrose and borage oil; ion-exchange water softeners; protease inhibitor SRD441 (Serentis Ltd); furfuryl palmitate in emollient; cipamfylline cream; andMycobacterium vaccaevaccine. Additional research evidence is needed for emollients, bath additives, antibacterials, specialist clothing and complementary and alternative therapies. There was no RCT evidence for topical corticosteroid dilution, impregnated bandages, soap avoidance, bathing frequency or allergy testing.LimitationsThe large scope of the review coupled with the heterogeneity of outcomes precluded formal meta-analyses. Our conclusions are still limited by a profusion of small, poorly reported studies.ConclusionsAlthough the evidence base of RCTs has increased considerably since the last NIHR HTA systematic review, the field is still severely hampered by poor design and reporting problems including failure to register trials and declare primary outcomes, small sample size, short follow-up duration and poor reporting of risk of bias. Key areas for further research identified by the review include the optimum use of emollients, bathing frequency, wash products, allergy testing and antiseptic treatments. Perhaps the greatest benefit identified is the use of twice weekly anti-inflammatory treatment to maintain disease remission. More studies need to be conducted in a primary care setting where most people with eczema are seen in the UK. Future studies need to use the same core set of outcomes that capture patient symptoms, clinical signs, quality of life and the chronic nature of the disease.FundingThe National Institute for Health Research Programme Grants for Applied Research programme.

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“…Leung et al reported that S. aureus isolated from lesional skin of more than half of their patients with AD could secrete toxins with the characteristics of SAgs (13). The SAgs of S. aureus are composed of enterotoxins (SEA, SEB, SEC), exofoliative toxins (ETA, ETB), and TSST-1 (14). Furthermore, these SAgs trigger the immunologic responses mediated by cytokines, resulting in inflammation of tissues (6)(7)(8)15).…”

Section: Discussionmentioning

confidence: 99%

Roles of SEA-expressing Staphylococcus aureus, isolated from an atopic dermatitis patient, on expressions of human β-defensin-2 and inflammatory cytokines in HaCaT cells

Cho

Cho²,

Lee³

2009

Int J Mol Med

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Abstract.Atopic dermatitis (AD) shows an increased susceptibility to Staphylococcus aureus infection partly due to decreased expression of human ß-defensin-2 (HBD-2). Interestingly, it was reported that the nasal carrier S. aureus down-regulates the expression of HBD-2 and -3, thereby the carrier strains of S. aureus retain an advantage to epithelial colonization and infection. In this study, we tried to isolate and characterize S. aureus from an AD patient, with recurrent oozing on his face. We studied the increased expression of inflammatory cytokines, such as IL-1ß, -6, -8, and TNF-· in S. aureus treated-HaCaT cells, which are mediated by secreting superantigens (SAgs), structural component, or both. In addition, we investigated whether the SAgs from S. aureus can downregulate the expression of HBD-2 in HaCaT cells making favorable conditions for colonization on skin. Our data showed that the isolated S. aureus has the exotoxin gene, sea exotoxin. The SEA producing-S. aureus induced the expression of IL-1ß, -6, -8 cytokines, and TNF-· in HaCaT cells. The expression of HBD-2 was increased in S. aureus-treated HaCaT cells. Furthermore IL-8 was also induced by the structure component of S. aureus. Taken together, the SEA producing S. aureus induced the up-regulation of pro-inflammatory cytokines as well as HBD-2, thereby resulting in induction of the persistent eczematous skin lesions in AD. Thus, our data may give insight into understanding the pathogenesis by which S. aureus induces and aggravates eczematous skin lesions in AD.

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Role of Bacterial Pathogens in Atopic Dermatitis

Cited by 86 publications

References 146 publications

Skin and nasal vestibule colonisation by Staphylococcus aureus and its susceptibility to drugs in atopic dermatitis patients

Skin and nasal vestibule colonisation by Staphylococcus aureus and its susceptibility to drugs in atopic dermatitis patients

Scoping systematic review of treatments for eczema

Roles of SEA-expressing Staphylococcus aureus, isolated from an atopic dermatitis patient, on expressions of human β-defensin-2 and inflammatory cytokines in HaCaT cells

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