Many patients are currently suffering from nickel (Ni)-induced allergic contact dermatitis (ACD). There have been few Korean studies dealing with the threshold of Ni-induced ACD and quantifying the total amount of Ni in the metal alloys. The aim of this study is to evaluate the amount of Ni leached from metal alloys and Ni contents in metal alloys, and to estimate the threshold of Ni-induced ACD. All the earrings we examined leached below 0.5 microgram/cm(2)/week, the upper limit of European Union (EU) regulation, but the other metal alloys leached a much higher amount of Ni than the limit. Likewise, all the earrings we examined contained less than 0.05% Ni (500 microgram/g), the upper limit of EU regulation, but the other metal alloys exceeded this limit. Twenty Ni-sensitive subjects, who were patch-tested with various concentrations of Ni sulphate, showed positive reactions to 5% and 1% Ni sulphate, 10 subjects showed positive reactions to 0.01%, and the most sensitive subject showed reaction even to 0.0001%. The subjects in this study were more sensitive to Ni than those in the previous studies done in Europe. Taken together, strictly regulating the Ni-containing alloys that are made in Korea is needed to lower the occurrence of Ni-induced ACD.
Alloys/*chemistry ; Dermatitis, Allergic Contact/*metabolism ; Dermatitis, Contact/*diagnosis/*etiology ; European Union ; Humans ; Irritants ; Korea ; Metals/*chemistry ; Nickel/*analysis ; Patch Tests ; Petrolatum ; Quality Control ; Time Factors

OBJECTIVES: Ozone is widely applied to treat allergic skin diseases such as eczema, atopic dermatitis, and contact dermatitis. However, the specific mechanism remains unclear. This study aims to investigate the effects of ozonated oil on treating 2,4-dinitrochlorobenzene (DNCB)-induced allergic contact dermatitis (ACD) and the underling mechanisms. METHODS: Besides the blank control (Ctrl) group, all other mice were treated with DNCB to establish an ACD-like mouse model and were randomized into following groups: a model group, a basal oil group, an ozonated oil group, a FcεRI-overexpressed plasmid (FcεRI-OE) group, and a FcεRI empty plasmid (FcεRI-NC) group. The basal oil group and the ozonated oil group were treated with basal oil and ozonated oil, respectively. The FcεRI-OE group and the FcεRI-NC group were intradermally injected 25 µg FcεRI overexpression plasmid and 25 µg FcεRI empty plasmid when treating with ozonated oil, respectively. We recorded skin lesions daily and used reflectance confocal microscope (RCM) to evaluate thickness and inflammatory changes of skin lesions. Hematoxylin-eosin (HE) staining, real-time PCR, RNA-sequencing (RNA-seq), and immunohistochemistry were performed to detct and analyze the skin lesions. RESULTS: Ozonated oil significantly alleviated DNCB-induced ACD-like dermatitis and reduced the expressions of IFN-γ, IL-17A, IL-1β, TNF-α, and other related inflammatory factors (all P<0.05). RNA-seq analysis revealed that ozonated oil significantly inhibited the activation of the DNCB-induced FcεRI/Syk signaling pathway, confirmed by real-time PCR and immunohistochemistry (all P<0.05). Compared with the ozonated oil group and the FcεRI-NC group, the mRNA expression levels of IFN-γ, IL-17A, IL-1β, IL-6, TNF-α, and other inflammatory genes in the FcεRI-OE group were significantly increased (all P<0.05), and the mRNA and protein expression levels of FcεRI and Syk were significantly elevated in the FcεRI-OE group as well (all P<0.05). CONCLUSIONS Ozonated oil significantly improves ACD-like dermatitis and alleviated DNCB-induced ACD-like dermatitis via inhibiting the FcεRI/Syk signaling pathway.
Animals ; Mice ; Dinitrochlorobenzene/metabolism* ; Skin/metabolism* ; Cytokines/metabolism* ; Interleukin-17/metabolism* ; Tumor Necrosis Factor-alpha/metabolism* ; Dermatitis, Allergic Contact/pathology* ; Dermatitis, Atopic/chemically induced* ; Signal Transduction ; RNA, Messenger/metabolism* ; Mice, Inbred BALB C

OBJECTIVESTo study the contact allergenic activities of trichloroethylene (TCE) and its three metabolites trichloroacetic acid, trichloroethanol and chloral hydrate.

METHODSA modified guinea pig maximization test (GPMT) was adopted. The skin sensitization (edema and erythema) was observed in trichloroethylene, trichloroacetic acid, trichloroethanol, chloral hydrate and 2,4-dinitrochlorobenzene.

RESULTSThe allergenic rate of TCE, trichloroacetic acid and 2,4-dinitrochlorobenzene was 71.4%, 58.3% and 100.0% respectively, and that of trichloroethanol and chloral hydrate was 0%. The mean response score of TCE, trichloroacetic acid and 2,4-dinitrochlorobenzene was 2.3, 1.1, 6.0 respectively. The histopathological analysis also showed an induction of allergenic transformation in guinea pig skin by both TCE and trichloroacetic acid.

CONCLUSIONTCE appears to be a strong allergen while trichloroacetic acid a moderate one. On the other hand, both trichloroethanol and chloral hydrate are weak sensitization potentials. Immunologic reaction induced by TCE might be postulated as the pathological process of this illness. Consequently, it is suggested that in the mechanism of Occupational Dermatitis Medicamentose-Like (ODML) induced by TCE, the chemical itself might be the main cause of allergy. As one of its metabolic products, trichloroacetic acid might be a subordinate factor.

Allergens ; toxicity ; Animals ; Chloral Hydrate ; toxicity ; Dermatitis, Allergic Contact ; etiology ; immunology ; Dermatitis, Irritant ; etiology ; immunology ; Ethylene Chlorohydrin ; analogs & derivatives ; toxicity ; Guinea Pigs ; Skin ; drug effects ; immunology ; Toxicity Tests ; Trichloroacetic Acid ; toxicity ; Trichloroethylene ; metabolism ; toxicity

OBJECTIVETo investigate the therapeutic effect of mustard seed on allergic contact dermatitis (ACD) in mice and explore the mechanism.

METHODSEighteen BALB/c mice were randomly divided into normal control group, model group and mustard seed group. The mice in the normal control group and model group were fed with normal chow, and those in mustard seed group were given 5% mustard seed mixed in the chow. Three weeks later, ACD was induced on the ear using 2, 4-dinitrofluorobenzene. After 24 h, the swelling of the ear was examined, and the rats were sacrificed to collect the ear tissue ears and blood for histopathological and immunohistochemical examinations, RT-PCR and enzyme-linked immunosorbent assay.

RESULTSIn mice with ACD, feeding with mustard seeds significantly lessened the ear swelling, improved the tissue histopathology, lowered the number of infiltrating Langerhans cells, and reduced the expressions of IL-1β, TNF-α and IL-6 mRNA in the ear, but did not cause significant changes in serum levels of IL-4, IFN-γ and IL-17.

CONCLUSIONMustard seed inhibits ACD in mice possibly by suppressing the expressions of IL-1β, TNF-α and IL-6 mRNA and inhibiting Langerhans cell migration in the epidermis.

Animals ; Dermatitis, Allergic Contact ; drug therapy ; metabolism ; Dinitrofluorobenzene ; adverse effects ; Female ; Interleukin-1beta ; metabolism ; Interleukin-6 ; metabolism ; Mice ; Mice, Inbred BALB C ; Mustard Plant ; Seeds ; Tumor Necrosis Factor-alpha ; metabolism

This study is to observe the inhibition of etoposide on allergic contact dermatitis (ACD) and explore its possible mechanism of action. Dinitrofluorobenzene was used to induce the allergic contact dermatitis in mouse ear. Three groups of animals were orally administrated with different doses of VP-16 (5, 10, and 20 mg x kg(-1)), separately, for six days. The degree of skin inflammatory reaction was observed by optical microscope. Expression of intercellular adhesion molecule (ICAM-1) was detected by immunohistochemical staining. Radioimmunoassay was applied to measure the serum level of tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10). VP-16 significantly decreased inflammatory cell infiltration and the degree of infiltration reaction, and decreased the level of TNF-a in serum and the expression of ICAM-l in skin. VP-16 can significantly inhibit allergic contact dermatitis induced by DNFB. This therapeutic effect of VP-16 on murine ACD may be due to inhibiting expression of some cytokines.
Animals ; Anti-Inflammatory Agents ; pharmacology ; Dermatitis, Allergic Contact ; blood ; etiology ; metabolism ; Dinitrofluorobenzene ; Etoposide ; pharmacology ; Female ; Intercellular Adhesion Molecule-1 ; metabolism ; Interleukin-10 ; blood ; Male ; Mice ; Random Allocation ; Skin ; metabolism ; Tumor Necrosis Factor-alpha ; blood

OBJECTIVETo investigate the effect of modified Yupingfeng granule on nuclear factor-kappaB (NF-kappaB)expression in mice with allergic contact dermatitis (ACD).

METHODSMouse models of ACD were treated with the granules at low, medium and high doses, with normal saline and hydrocortisone as the negative and positive controls, respectively. The expressions of NF-kappaB and its distribution in the lesions were detected using immunohistochemistry.

RESULTSThe staining intensity, area and positive expression rates of NF-kappaB p50 were significantly different between the treatment group and the normal saline group (P<0.05).

CONCLUSIONModified Yupingfeng granule can effectively inhibit the expression of NF-kappaB in ACD, which might be a possible mechanism for its therapeutic effect on ACD.

Animals ; Dermatitis, Allergic Contact ; drug therapy ; metabolism ; Dose-Response Relationship, Drug ; Drugs, Chinese Herbal ; administration & dosage ; pharmacology ; therapeutic use ; Gene Expression Regulation ; drug effects ; Mice ; Mice, Inbred BALB C ; NF-kappa B ; metabolism

This study is to elucidate the immunoregulation mechanisms of artesunate (AST) on allergic contact dermatitis (ACD). Pharmacodynamics analyses, HE staining, semi-quantitative RT-PCR and Western blotting were used to explore the effects of AST on the related cytokines, transcription factor and signaling molecule of ACD respectively. The results indicated that topical administration of AST not only reduced the increase of ear swelling, spleen index and inflammatory cells infiltration in ACD mice, but also inhibited remarkably the expression of IFN-gamma, T-bet and NF-kappaB p65. It's suggested that AST could exhibit suppressive effects on inflammatory response and immune function of ACD, which indicates the possibility of developing AST as a novel immunoregulatory agent in the treatment of ACD and other immune-related diseases.
Administration, Topical ; Animals ; Artemisinins ; administration & dosage ; chemistry ; pharmacology ; Dermatitis, Allergic Contact ; immunology ; metabolism ; pathology ; Ear ; pathology ; Female ; GATA3 Transcription Factor ; genetics ; metabolism ; Hypersensitivity, Delayed ; drug therapy ; Immunosuppressive Agents ; administration & dosage ; chemistry ; pharmacology ; Interferon-gamma ; genetics ; metabolism ; Interleukin-4 ; genetics ; metabolism ; Mice ; Mice, Inbred ICR ; Molecular Structure ; NF-kappa B ; metabolism ; RNA, Messenger ; metabolism ; T-Box Domain Proteins ; genetics ; metabolism

OBJECTIVETo evaluate the effect of panaxynol (PAN) on delayed type hypersensitivity and possible mechanism.

METHODAllergic contact dermatitis (ACD) was induced by DNCB as a delayed type hypersensitivity (DTH) model to observe effect of PAN on auricle inflammation including pathological injury. Proliferation of T lymphocytes was induced by ConA and measured by MTf method. IFN-gamma secretion of splenocyte induced by ConA was detected by ELISA.

RESULTThe swelling degree of auricle and pathological injury in ACD mice was reduced significantly by treated with PAN in induction phase. Proliferation of T lymphocytes induced by ConA in vitro was inhibited significantly by PAN, By contrast, no detectable effect was observed in resting splenocyte. IFN-y induced by ConA in splenocytes was inhibited markedly by PAN from 10 micromol x L(-1) and from 6 h.

CONCLUSIONThe results showed that DTH was inhibited by PAN mainly in induction phase and this effect may be related with the inhibition on T lymphocytes proliferation and secretion of IFN-gamma.

Animals ; Cell Proliferation ; drug effects ; Concanavalin A ; metabolism ; Dermatitis, Allergic Contact ; drug therapy ; immunology ; metabolism ; Diynes ; pharmacology ; therapeutic use ; Fatty Alcohols ; pharmacology ; therapeutic use ; Female ; Interferon-gamma ; secretion ; Male ; Mice ; Mice, Inbred ICR ; Spleen ; drug effects ; pathology ; secretion ; T-Lymphocytes ; drug effects ; pathology