961 Colonization of a 3D skin model with a complete microbiota is more beneficial to the skin barrier than with Staphylococcus epidermidis alone (original) (raw)
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The Journal of Dermatology, 2000
The expression of Heat Shock Protein (HPS) 72/73, HSP65 and HSP27 in skin lesions of atopic dermatitis (n=21) was studied and compared with that in contact dermatitis (n=18) and normal skin (n=9). Keratinocytes in the whole epidermis expressed both HSP65 and HSP72/73 with a membranous, cytoplasmic or nuclear/perinuclear staining pattern much more intensely in atopic dermatitis than in contact dermatitis and normal subjects. In approximately half of the subjects with atopic dermatitis, infiltrating cells in the dermis expressed HSP~5 and HSP72/73; this was not observed in contact dermatitis. HSP27 was expressed in the upper epidermis with a cytoplasmic or nuclear/perinuclear staining pattern in all groups. HSP27 was not expressed by infiltrating cells. A clinical evaluation of atopic dermatitis showed that more severe types of atopic dermatitis expressed more intense expression of HSP65 and HSP72/73, but not HSP27, in their skin lesions. These findings suggested that HSP65 and HSP72/73 may play roles in the pathogenesis of atopic dermatitis.
Transcriptional landscape of psoriasis identifies the involvement of IL36 and IL36RN
Background: In present study we performed whole transcriptome analysis in plaque psoriasis patients and compared lesional skin with non-lesional skin and with the skin from healthy controls. We sequenced total RNA from 12 lesional (LP), 12 non-lesional (NLP) and from 12 normal (C) skin biopsies. Results: Compared with previous gene expression profiling studies we had three groups under analysis - LP, NLP and C. Using NLP samples allows to see the transcriptome of visually normal skin from psoriasis patient. In LP skin S100A12, S100A7A, LCE3E, DEFB4A, IL19 were found up regulated. In addition to already these well-described genes, we also found several other genes related to psoriasis. Namely, KLK9, OAS2, OAS3, PLA2G, IL36G, IL36RN were found to be significantly and consistently related to the psoriatic lesions and this finding is supported also by previous studies. The genes up-regulated in the LP samples were related to the innate immunity, IL17 and IL10 networks. In NLP samples innate immunity and IL17 network were activated, but activation of IL10 network was not evident. The transcriptional changes characteristic in the NLP samples can be considered as a molecular signature of “dormant psoriasis”. Conclusions: Taken together, our study described the transcriptome profile characteristic for LP and NLP psoriatic skin. RNA profile of the NLP skin is in between the lesional and healthy skin, with its own specific pattern. We found that both LP and NLP have up-regulated IL17 network, whereas LP skin has up regulated IL10 related cytokines (IL19, IL20, IL24). Moreover, IL36G and IL36RN were identified as strong regulators of skin pathology in both LP and NLP skin samples, with stronger influence in LP samples.
The Journal of Immunology, 2010
Keratinocytes play a crucial role in the regulation of skin inflammation, responding to environmental and immune cells stimuli. They produce soluble factors that can act in an autocrine or paracrine manner on immune cells or directly on aggressors. A screening of the activities of 36 cytokines on keratinocyte gene expression identified IL-17A, IL-22, oncostatin M, TNF-a, and IL-1a as potent cytokines in inducing cutaneous inflammation. These five proinflammatory cytokines synergistically increased production of CXCL8 and b-defensin 2 (BD2). In addition, ex vivo studies on human skin explants demonstrated upregulation of BD2, S100A7, and CXCL8 expression in response to the same combination of cytokines. In vivo intradermal injection of these five cytokines in mouse increased CXCL1, CXCL2, CXCL3, S100A9, and BD3 expression, associated with neutrophil infiltration. We confirmed and extended this synergistic effect using quantitative real-time PCR analysis and observed increased expression of nine chemokines and 12 antimicrobial peptides. Production of CXCL, CXCL5, and CXCL8 by keratinocytes stimulated in the presence of this cytokine combination was associated with increased neutrophil chemotactic activity. Similarly, high production of BD2, BD3, and S100A7 was associated with an increased antimicrobial activity. Finally, the transcriptional profile observed in this in vitro model of inflammatory keratinocytes correlated with the one of lesional psoriatic skin. Our results demonstrate the important potentiating activities of IL-17A, IL-22, oncostatin M, TNF-a, and IL-1a on keratinocytes. This is particularly interesting in the context of psoriasis where these cytokines are overexpressed and could synergize to play an important role in upregulation of chemokines and antimicrobial peptides production.
The Journal of Dermatology, 1993
Biopsied specimens from skin lesions ofSLE were studied for expression of 70 KDheat shock protein (HSP70). The pattern of HSP70 expression in SLE was diffuse in whole epidermis, hair follicles, and sweat gland cells and rather more intense than that in other control groups or normal skin. No significant differences in HSP70 expression were observed between sun-exposed and protected areas of SLE skin lesions. Unlike SLE, reduced or no expression of HSP70 was observed in skin lesions of DLE. In tissue culture, UVB radiation in vitro induced relatively intense expression of HSP70 in the nuclear area ofkeratinocytes. A few yOT cell receptor positive cells which might respond to HSP70 expressing cells were detected in the basal layer of skin lesions of diseases. These studies suggest that abberant expression of HSP70 in skin lesions of SLE might contribute to both skin lesions and antibody formation in SLE.