Nickel allergic contact dermatitis.
Ontology highlight
ABSTRACT:
SUBMITTER: Zhu M
PROVIDER: S-EPMC9435531 | biostudies-literature | 2022 Aug
REPOSITORIES: biostudies-literature
Publications
Nickel allergic contact dermatitis.
Zhu Mingang M Vinturache Angela A Ding Guodong G
CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne 20220801 33
Similar Datasets
Project description:This SuperSeries is composed of the SubSeries listed below.
2015-10-01 | GSE58817 | GEO
Project description:We found that keratinocytes (KCs) (from healthy subjects) stimulated with nickel were characterized by a specific miRNA signature that were different from vehicle-stimulated KCs.
2015-10-01 | GSE58816 | GEO
Project description:We found that peripheral blood mononuclear cells (PBMCs) (from subjects with allergy to nickel) stimulated with nickel were characterized by a specific miRNA signature that were different from vehicle-stimulated PBMCs.
2015-10-01 | GSE58815 | GEO
Project description:Our findings demonstrate that nickel-challenged skin in subjects with allergy to nickel is characterized by a specific miRNA signature compared to vehicle-challenged skin. In addition, we found that miRNA expression changes are different in allergic contact dermatitis (ACD to nickel) compared to irritant contact dermatitis (ICD).
2015-10-01 | GSE58814 | GEO
Project description:Allergic contact dermatitis (ACD) is well recognized as an adverse event associated with implantable medical devices that contain allergenic materials like nickel; however, other cutaneous consequences of chronic exposure to allergens in implanted devices are not well understood. Here, we present a clinical case of Marjolin's ulcer, an invasive squamous cell carcinoma (SCC) that developed in response to chronic ACD caused by an orthopedic implant. We used a standard murine model of contact hypersensitivity to determine whether chronic ACD promotes skin carcinogenesis. Chronic application of 1-fluoro-2,4-dinitrobenzene (DNFB) to carcinogen-treated skin led to the development of papillomas and aggressive SCC. DNFB-driven chronic ACD was marked by type 2 inflammation, which mediated skin carcinogenesis, as mice unable to mount an inflammatory response were less likely to develop skin tumors. Importantly, we found similar tumor-promoting inflammation surrounding the SCC in our patient. Our findings demonstrate that chronic ACD caused by constant exposure to an allergen can promote tumorigenesis at skin sites with preexisting cancer-initiated cells. Moreover, our results suggest that patients with implantable devices placed in close proximity to the skin should be monitored for ACD and highlight the importance of patch testing prior to the placement of such devices.
| S-EPMC4347218 | biostudies-literature
Project description:Allergic contact dermatitis (ACD) is a common inflammatory skin disease with a prevalence of approximately 20% in the European population. ACD is caused by contact allergens that are reactive chemicals able to modify non-immunogenic self-proteins to become immunogenic proteins. The most frequent contact allergens are metals, fragrances, and preservatives. ACD clinically manifests as pruritic eczematous lesions, erythema, local papules, and oedema. ACD is a T cell-mediated disease, involving both CD4+ and CD8+ T cells. In addition, ?? T cells appear to play an important role in the immune response to contact allergens. However, it is debated whether ?? T cells act in a pro- or anti-inflammatory manner. A special subset of ?? T cells, named dendritic epidermal T cells (DETC), is found in the epidermis of mice and it plays an important role in immunosurveillance of the skin. DETC are essential in sensing the contact allergen-induced stressed environment. Thus, allergen-induced activation of DETC is partly mediated by numerous allergen-induced stress proteins expressed on the keratinocytes (KC). Several stress proteins, like mouse UL-16-binding protein-like transcript 1 (Mult-1), histocompatibility 60 (H60) and retinoic acid early inducible-1 (Rae-1) ?-? family in mice and major histocompatibility complex (MHC) class I-chain-related A (MICA) in humans, are upregulated on allergen-exposed KC. Allergen-induced stress proteins expressed on the KC are consequently recognized by NKG2D receptor on DETC. This review focuses on the role of ?? T cells in ACD, with DETC in the spotlight, and on the role of stress proteins in contact allergen-induced activation of DETC.
| S-EPMC7248261 | biostudies-literature
Project description:BackgroundLong-term use of most immunosuppressants to treat allergic contact dermatitis (ACD) generates unavoidable severe side effects, warranting discovery or development of new immunosuppressants with good efficacy and low toxicity is urgently needed to treat this condition. Hispidulin, a flavonoid compound that can be delivered topically due to its favorable skin penetrability properties, has recently been reported to possess anti-inflammatory and immunosuppressive properties. However, no studies have investigated the effect of hispidulin on Th1 cell activities in an ACD setting.MethodsA contact hypersensitivity (CHS) mouse model was designed to simulate human ACD. The immunosuppressive effect of hispidulin was investigated via ear thickness, histologic changes (i.e., edema and spongiosis), and interferon-gamma (IFN-γ) gene expression in 1-fluoro-2,4-dinitrobenzene (DNFB)-sensitized mice. Cytotoxicity, total number of CD4+ T cells, and percentage of IFN-γ-producing CD4+ T cells were also investigated in vitro using isolated CD4+ T cells from murine spleens.ResultsTopically applied hispidulin effectively inhibited ear swelling (as measured by reduction in ear thickness), and reduced spongiosis, IFN-γ gene expression, and the number of infiltrated immune cells. The inhibitory effect of hispidulin was observed within 6 h after the challenge, and the observed effects were similar to those effectuated after dexamethasone administration. Hispidulin at a concentration up to 50 μM also suppressed IFN-γ-producing CD4+ T cells in a dose-dependent manner without inducing cell death, and without a change in total frequencies of CD4+ T cells among different concentration groups.ConclusionThe results of this study, therefore, suggest hispidulin as a novel compound for the treatment of ACD via the suppression of IFN-γ production in Th1 cells.
| S-EPMC6792202 | biostudies-literature
Project description: Not available
| S-EPMC8651521 | biostudies-literature
Project description:Allergic and irritant contact dermatitis induces different immunological cascades, involving a plethora of immune cells as well as keratinocytes. This highly interwoven network is regulated by miRNAs. However, which miRNAs are involved during allergic- and irritant-induced contact dermatitis is not well investigated. Therefore, we analyzed miRNA and mRNA expression data of the same sample from positive patch test reactions from 27 patients topically exposed to allergens (nickel (Ni), epoxy resin (EP) and methylchloroisothiazolinone (CM); each n=5), irritants (sodium lauryl sulfate (SL, n=9) and nonanoic acid (NO, n=5)), as well as healthy skin (n=5).
2020-07-01 | E-MTAB-9026 | biostudies-arrayexpress
Project description:Allergic and irritant contact dermatitis induces different immunological cascades, involving a plethora of immune cells as well as keratinocytes. This highly interwoven network is regulated by miRNAs. However, which miRNAs are involved during allergic- and irritant-induced contact dermatitis is not well investigated. Therefore, we analyzed miRNA and mRNA expression data of the same sample from positive patch test reactions from 27 patients topically exposed to allergens (nickel (Ni), epoxy resin (EP) and methylchloroisothiazolinone (CM); each n=5), irritants (sodium lauryl sulfate (SL, n=9) and nonanoic acid (NO, n=5)), as well as healthy skin (n=5). This is the mRNA dataset for these experiments.
2020-07-01 | E-MTAB-9051 | biostudies-arrayexpress