Adhesion of Staphylococcus aureus to horny layer: role of fibrinogen

Kanzaki, Hiromitsu; Morishita, Yoshiko; Akiyama, Hisanori; Arata, Jirô

doi:10.1016/0923-1811(95)00472-6

Cited by 15 publications

(5 citation statements)

References 14 publications

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“…74,75 Application of S aureus directly onto mouse skin is sufficient to cause a dermatitis phenotype that can be exacerbated with prior tape stripping to disrupt the skin barrier or occlusive dressings to maximize the colonization. 76,77 Topical application of S aureus isolates cultivated from patients with AD directly inoculated onto mice was sufficient to induce epidermal thickening and inflammatory responses compared with S aureus from healthy control subjects. 78 The mechanism of action by which S aureus elicits dermatitis and inflammatory phenotypes is multifactorial and intertwined with microbial community dynamics.…”

Section: Skin Microbiome and Microbial Alterations In Patients With Admentioning

confidence: 99%

Insights into atopic dermatitis gained from genetically defined mouse models

Nakajima

Nomura

Common

et al. 2019

Journal of Allergy and Clinical Immunology

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Atopic dermatitis (AD) is characterized by severe pruritus and recurrent eczema with a chronic disease course. Impaired skin barrier function, hyperactivated T H 2 cell-type inflammation, and pruritus-induced scratching contribute to the disease pathogenesis of AD. Skin microbial alterations complicate the pathogenesis of AD further. Mouse models are a powerful tool to analyze such intricate pathophysiology of AD, with a caution that anatomy and immunology of the skin differ between human subjects and mice. Here we review recent understanding of AD etiology obtained using mouse models, which address the epidermal barrier, skin microbiome, T H 2 immune response, and pruritus.

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Section: Skin Microbiome and Microbial Alterations In Patients With Admentioning

confidence: 99%

Insights into atopic dermatitis gained from genetically defined mouse models

Nakajima

Nomura

Common

et al. 2019

Journal of Allergy and Clinical Immunology

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“…Nonadherent bacteria are commonly removed by washing, filtration or differential centrifugation, and adhesion is then quantified either by direct visualization under light or electron microscopy or by the use of markers such as fluorescent dyes or radioactivity. [13][14][15][16] The limitations of many adherence assays include extended time for analysis, operator fatigue, subjectivity, and in the case of radiometric assays, an inability to discriminate between bacteria specifically adhering to tissue and those attached to the inert support. 11 Image analysis techniques have been employed which have helped to minimize some of these limitations.…”

Section: Introductionmentioning

confidence: 99%

Staphylococcal and micrococcal adherence to canine and feline corneocytes: quantification using a simple adhesion assay

Lu¹,

McEwan²

2007

Veterinary Dermatology

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In this paper a simple adhesion assay suitable for the assessment of bacterial adhesion to both canine and feline corneocytes is described. Using this assay Staphylococcus intermedius, Staphylococcus aureus and Staphylococcus chromogenes were shown to adhere well to both canine and feline corneocytes. The numbers of adherent bacteria were, however, generally lower for feline corneocytes. Both Staphylococcus hominis and a Micrococcus species adhered poorly to canine and feline corneocytes. This is the first report documenting bacterial adhesion to feline corneocytes.

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“…Well‐described attachment factors to human keratinocytes include staphylococcal protein A, clumping factor and fibronectin‐binding protein 11 . Further ligands, especially the matrix‐protein binding structures (including laminin‐binding protein, vitronectin‐binding protein and collagen‐binding protein) and fibrinogen are currently under debate 12–15 . After establishing the contact with epidermal cells, the staphylococcal α‐toxin has been described to cause fatal cell damage to human keratinocytes by forming transmembrane pores, which consist of six subunits and, after aggregation on the cell surface, enable the passage of monovalent ions through the cellular membrane followed by a breakdown of the cellular adenosine triphosphate metabolism 16,17 .…”

mentioning

confidence: 99%