Defects of filaggrin-like proteins in both lesional and nonlesional atopic skin

Pellerin, Laurence; Henry, Julie; Hsu, Chiung-Yueh; Balica, S.; Jean‐Decoster, Catherine; Méchin, Marie-Claire; Hansmann, Britta; Rodríguez, Elke; Weindinger, Stefan; Schmitt, Anne-Marie; Serre, Guy; Paul, C.; Simon, Michel

doi:10.1016/j.jaci.2012.12.1566

Cited by 216 publications

(239 citation statements)

References 48 publications

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“…This is consistent with the clinical observation that filaggrin expression is significantly lower in the lesional AD, as compared to nonlesional AD skin (43). IL-4 and IL-13, together with TNF-α, also increase the expression of glucocorticoid-induced TNF receptor-related protein ligand in keratinocytes (44).…”

Section: Pathogenesis Of Atopic Dermatitissupporting

confidence: 89%

New insights in the pathogenesis of atopic dermatitis

Ong

2013

Pediatr Res

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Section: Pathogenesis Of Atopic Dermatitissupporting

confidence: 89%

New insights in the pathogenesis of atopic dermatitis

Ong

2013

Pediatr Res

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“…The cornified envelope proteins loricrin and cytokeratin 10 are ligands for ClfB, and it may be through binding to these proteins that ClfB mediates bacterial attachment to corneocytes. Alternatively, given the altered corneocyte morphology and protein expression profiles in AD skin, where NMF levels are low (12,28,29), it is possible that ClfB binds to other protein ligands. Additional S. aureus factors are likely to contribute to the adhesion of S. aureus to corneocytes and the colonization of AD skin.…”

Section: Discussionmentioning

confidence: 99%

Clumping Factor B Promotes Adherence of Staphylococcus aureus to Corneocytes in Atopic Dermatitis

et al. 2017

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Staphylococcus aureus skin infection is a frequent and recurrent problem in children with the common inflammatory skin disease atopic dermatitis (AD). S. aureus colonizes the skin of the majority of children with AD and exacerbates the disease. The first step during colonization and infection is bacterial adhesion to the cornified envelope of corneocytes in the outer layer, the stratum corneum. Corneocytes from AD skin are structurally different from corneocytes from normal healthy skin. The objective of this study was to identify bacterial proteins that promote the adherence of S. aureus to AD corneocytes. S. aureus strains from clonal complexes 1 and 8 were more frequently isolated from infected AD skin than from the nasal cavity of healthy children. AD strains had increased ClfB ligand binding activity compared to normal nasal carriage strains. Adherence of single S. aureus bacteria to corneocytes from AD patients ex vivo was studied using atomic force microscopy. Bacteria expressing ClfB recognized ligands distributed over the entire corneocyte surface. The ability of an isogenic ClfB-deficient mutant to adhere to AD corneocytes compared to that of its parent clonal complex 1 clinical strain was greatly reduced. ClfB from clonal complex 1 strains had a slightly higher binding affinity for its ligand than ClfB from strains from other clonal complexes. Our results provide new insights into the first step in the establishment of S. aureus colonization in AD patients. ClfB is a key adhesion molecule for the interaction of S. aureus with AD corneocytes and represents a target for intervention.

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“…The epidermal calcium ion gradient is also disturbed in AD (14), and in certain cases, alterations in the levels of Filaggrin; a key calcium-dependent protein in skin-barrier formation which may predispose subjects to the disease (15). Recently, the levels of the S100 proteins, Hornerin and Filaggrin 2 were shown to be decreased in the epidermis of patients with AD (16).…”

Section: Introductionmentioning

confidence: 99%

Calmodulin‐like skin protein level increases in the differentiated epidermal layers in atopic dermatitis

Donovan

Ambach

Thomas-Collignon

et al. 2013

Experimental Dermatology

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In atopic dermatitis (AD), the skin barrier is disturbed, and the expression of calcium-dependent S100 proteins and the calcium gradient is also altered in the epidermis. The calmodulinlike skin protein (CLSP), which is expressed in the differentiated epidermis, is believed to modulate the function of calciumdependent proteins involved in barrier formation and is significantly increased in the epidermis of psoriatic patients. We, therefore, investigated the CLSP level in skin biopsies taken from patients with acute exacerbated and non-exacerbated AD as well as from healthy control subjects. Immunohistochemical, Western blot and ELISA analyses showed significant increases (P < 0.03) in CLSP level in the epidermis from patients with acute exacerbated AD as compared to that from patients with non-exacerbated AD and from control subjects. Such increased expression of CLSP may help re-establish a functional epidermal barrier in acute AD.Abbreviations: AD, atopic dermatitis; CLSP, calmodulin-like skin protein; AEAD, acute exacerbated AD; NEAD, non-exacerbated AD.

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Defects of filaggrin-like proteins in both lesional and nonlesional atopic skin

Cited by 216 publications

References 48 publications

New insights in the pathogenesis of atopic dermatitis

New insights in the pathogenesis of atopic dermatitis

Clumping Factor B Promotes Adherence of Staphylococcus aureus to Corneocytes in Atopic Dermatitis

Calmodulin‐like skin protein level increases in the differentiated epidermal layers in atopic dermatitis

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