Inflammatory plasma signature of chronic hand eczema: Associations with aetiological and clinical subtypes.

BACKGROUND: Chronic hand eczema (CHE) is a highly prevalent, heterogeneous, skin disease that encompasses different aetiological and clinical subtypes. Severe CHE without atopic dermatitis has been associated with systemic inflammation; yet it remains unknown if specific CHE subtypes leave distinct, systemic, molecular signatures. OBJECTIVES: To characterize the inflammatory plasma signature of different aetiological and clinical CHE subtypes. METHODS: We assessed expression levels of 266 inflammatory and cardiovascular disease risk plasma proteins as well as filaggrin gene mutation status in 51 well-characterized CHE patients without concomitant atopic dermatitis and 40 healthy controls. Plasma protein expression was compared between aetiological and clinical CHE subgroups and controls both overall and according to clinical CHE severity. Correlation analyses for biomarkers, clinical and self-reported variables were performed. RESULTS: Very severe, chronic allergic contact dermatitis (ACD) on the hands was associated with a mixed Type 1/Type 2 systemic immune activation as compared with controls. Circulating levels of Type 1/Type 2 inflammatory biomarkers correlated positively with clinical disease severity among CHE patients with ACD. No biomarkers were found, that could discriminate between aetiological subtypes, for example, between ACD and irritant contact dermatitis. Hyperkeratotic CHE showed a distinct, non-atopic dermatitis-like, systemic footprint with upregulation of markers associated with Type 1 inflammation and tumour necrosis factor alpha, but not Type 2 inflammation. Increased levels of CCL19 and CXCL9/10 could discriminate hyperkeratotic CHE from both vesicular and chronic fissured CHE, whereas no difference was found between the latter two subtypes. CONCLUSION: Profiling of systemic biomarkers showed potential for identifying certain CHE subtypes. Peripheral blood levels of inflammatory biomarkers were associated and correlated with the clinical disease severity of chronic ACD on the hands, underlining that this is a systemic disease. We question whether hyperkeratotic CHE should be classified as eczema.

Potential classification of chemical immunologic response based on gene expression profiles.

Occupational immune diseases are a serious public health burden and are often a result of exposure to low molecular weight (LMW) chemicals. The complete immunological mechanisms driving these responses are not fully understood which has made the classification of chemical allergens difficult. Antimicrobials are a large group of immunologically-diverse LMW agents. In these studies, mice were dermally exposed to representative antimicrobial chemicals (sensitizers: didecyldimethylammonium chloride (DDAC), ortho-phthalaldehyde (OPA), irritants: benzal-konium chloride (BAC), and adjuvant: triclosan (TCS)) and the mRNA expression of cytokines and cellular mediators was evaluated using real-time qPCR in various tissues over a 7-days period. All antimicrobials caused increases in the mRNA expression of the danger signals Tslp (skin), and S100a8 (skin, blood, lung). Expression of the TH2 cytokine Il4 peaked at different timepoints for the chemicals based on exposure duration. Unique expression profiles were identified for OPA (Il10 in lymph node, Il4 and Il13 in lung) and TCS (Tlr4 in skin). Additionally, all chemicals except OPA induced decreased expression of the cellular adhesion molecule Ecad. Overall, the results from these studies suggest that unique gene expression profiles are implicated following dermal exposure to various antimicrobial agents, warranting the need for additional studies. In order to advance the development of preventative and therapeutic strategies to combat immunological disease, underlying mechanisms of antimicrobial-induced immunomodulation must be fully understood. This understanding will aid in the development of more effective methods to screen for chemical toxicity, and may potentially lead to more effective treatment strategies for those suffering from immune diseases.

Silkworm dropping extract ameliorate trimellitic anhydride-induced allergic contact dermatitis by regulating Th1/Th2 immune response.

Allergic contact dermatitis (ACD) is an inflammatory skin disease caused by hapten-specific immune response. Silkworm droppings are known to exert beneficial effects during the treatment of inflammatory diseases. Here, we studied whether topical treatment and oral administration of silkworm dropping extract (SDE) ameliorate trimellitic anhydride (TMA)-induced ACD. In ACD mice model, SDE treatment significantly suppressed the increase in both ear thickness and serum IgE levels. Furthermore, IL-1ß and TNF-α levels were reduced by SDE. In allergic responses, SDE treatment significantly attenuated the production of the Th2-associated cytokine IL-4 in both ear tissue and draining lymph nodes. However, it increased the production of the Th1-mediated cytokine IL-12. Thus, these results showed that SDE attenuated TMA-induced ACD symptoms through regulation of Th1/Th2 immune response. Taken together, we suggest that SDE treatment might be a potential agent in the prevention or therapy of Th2-mediated inflammatory skin diseases such as ACD and atopic dermatitis. ABBREVIATIONS: ACD: allergic contact dermatitis; AD: atopic dermatitis; APC: antigen presenting cells; CCL: chemokine (C-C motif) ligand; CCR: C-C chemokine receptor; Dex: dexamethasone; ELISA: enzyme-linked immunosorbent assay; IFN: interferon; Ig: immunoglobulin; IL: interleukin; OVA: ovalbumin; PS: prednisolone; SDE: silkworm dropping extract; Th: T helper; TMA: trimellitic anhydride; TNF: tumor necrosis factor.

Elevation of Circulating Th17/Th22 Cells Exposed to Low-Level Formaldehyde and Its Relevance to Formaldehyde-Induced Occupational Allergic Contact Dermatitis.

OBJECTIVES: The aim of this study was to investigate the effects of formaldehyde exposure on Th17 and Th22 cells and its relevance to human occupational allergic contact dermatitis (OACD). METHODS: Circulating IL17-/IL22-secreting cells and serum IL17/IL22 levels in formaldehyde-exposed workers at Occupational Exposure Limit and nonexposed controls were assessed. RESULTS: The IL17 and IL22 cell population were detected in both CD3CD8 and CD3CD8 cells. The percentages of circulating IL17 and IL22 T cells in the workers with and without ACD history were all elevated, which were more remarkable in the ones with ACD history. Serum levels of IL17 and IL22 between the workers and controls were not significantly different. CONCLUSIONS: Low-level formaldehyde exposure may increase circulating IL17-/IL22-producing T cells (CD8 and CD8), possibly involved in the development of human OACD. But it may not alter serum levels of IL17/IL22 before the appearance of OACD symptoms.

[Prediction of occupational allergic contact dermatitis induced by formaldehyde by IL17/IL22 secretion cell rest combined with patch test].

Objective: To investigate the possible role of IL17-and IL22-secreting cells combined with patch test for the prediction of formaldehyde-induced occupational allergic contact dermatitis(OACD). Methods: From October 2014 to October 2016, totally 131 formaldehyde-exposed workers(49 cases with inflammatory skin lesions,82 ones without inflammatory skin lesions)and 63 non-exposed health controls were recruited. Patch-test was performed in 49 cases of formaldehyde-exposed workers with inflammatory skin lesions. Circulating IL17+and IL22+Tcell subsets were assessed by flow cytometry(FCM). Results: Among 49 cases of formaldehyde-exposed workers with inflammatory skin lesions,32 cases were with positive patch-test while 17 cases with negative patch-test. The proportions of circulating CD3+CD8-IL17+ and CD3+CD8-IL22+ cells from patch-test(+) formaldehyde-exposed workers were significantly higher than that of patch-test(-)group, formaldehyde-exposed workers without skin lesions and non-exposed controls(P<0.05). The proportions of circulating CD3+CD8-IL17+ and CD3+CD8-IL22+cells from patch-test(-)group and formaldehyde-exposed workers without skin lesions were also higher than that of non-exposed controls(P<0.05). But there was no significant difference between patch-test(-)group and formaldehyde-exposed workers without skin lesions(P>0.05). Peripheral CD3+CD8+IL17+and CD3+CD8+IL22+cells were also detected in spite of small amounts. The percentages of CD3+CD8+IL17+and CD3+CD8+IL22+ cells inperipheral blood from patch-test(+)formaldehyde-exposed workers were enhanced significantly, compared to patch-test(-)group, formaldehyde-exposed workers without skin lesions and non-exposed controls(P<0.05). The proportions of circulating CD3+CD8+IL17+ and CD3+CD8+IL22+ cells from patch-test(-)group and formaldehyde-exposed workers without skin lesions were significantly higher than that of non-exposed controls(P<0.05). But there was no significant difference between patch-test(-) group and formaldehyde-exposed workers without skin lesions(P>0.05). Conclusion: The proportions of circulating IL17+ and IL22+T cells(both CD8-and CD8+)are enhanced in formaldehyde-exposed workers at proposed OEL, possibly involved in the development of formaldehyde-induced OACD.The detection of IL17-and IL22-secreting cells combined with formaldehyde patch test help to screen the workers with allergy property and prevent OACD.

Luminex LiquiChip System for the Evaluation of Cytokine Levels in Patients with Contact Dermatitis to Potassium Dichromate.

BACKGROUND: Allergic contact dermatitis (ACD) is associated with increased production of cytokines. The patch test is the "gold-standard" diagnostic method, but it poses a risk of false results. OBJECTIVE: To evaluate a novel laboratory technique, the Luminex LiquiChip, which simultaneously measures blood levels of multiple cytokines, as a diagnostic tool in patients with chrome-induced ACD. METHODS: The study group included 20 patients with ACD and relevant patch test results for potassium dichromate and 19 patients with ACD for nickel or fragrance as control. Peripheral blood mononuclear cells (PBMCs) were cultured in the presence and absence of potassium dichromate. The Luminex LiquiChip was used to measure levels of the following cytokines: granulocyte-macrophage colony-stimulating factor, interleukin (IL)-1ß, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, interferon-γ, and tumor necrosis factor (TNF)-α. RESULTS: Potassium dichromate-stimulated PBMCs secreted significantly higher amounts of all cytokines except TNF-α than nonstimulated PBMCs. PBMCs from patients with ACD to chromium secreted significantly higher amounts of all cytokines tested, except IL-4, compared to PBMCs from patients with ACD to nickel or fragrance. CONCLUSIONS: Potassium dichromate stimulates the production of both Th1- and Th2-type cytokines in patients with chrome allergy. The Luminex LiquiChip is a promising in vitro method and may serve as a diagnostic tool for ACD.

Nickel allergy: blood and periodontal evaluation after orthodontic treatment / Alergia ao níquel: avaliação periodontal e sanguínea após o tratamento ortodôntico

The aim of this study was to assess periodontal status and bloodparameters in orthodontic patients with nickel allergy one monthafter removal of brackets. Ninety-six randomly selected patientswere initially evaluated. Allergy to nickel was diagnosed using apatch test. After determining the prevalence of subjects allergic tonickel, two groups were formed: 16 allergic (experimental) and 16non-allergic (control) patients. Their periodontal status wasdetermined regularly by a single, blinded, duly calibrated examinerusing the Lõe Index (GI) and their blood was tested (complete bloodtest, including nickel and IgE levels) after nine months oforthodontic treatment and again one month after removing theorthodontic appliances. Statistical analyses included paired andnon-paired t-tests, Mann-Whitney, Wilcoxon, McNemar and lineartrend chi-square tests (p≤0.05). Comparison of the values recordedduring orthodontic treatment and one month after removing theappliances showed that in the allergic group there was significantincrease in eosinophils (p=0.046), basophils (p=0.001) andmonocytes (p=0.002), and decrease in number of bands (p=0.000),while in the control group, there was increase in lymphocytes(p=0.039) and decrease in segmented neutrophils (p=0.030) andIgE levels (p=0.001). In both groups, plasma nickel levels increased(p=0.010; p=0.039) and GI scores decreased. One month afterremoving the brackets, blood and periodontal parameters frompatients with and without nickel allergy were similar.

O objetivo do presente estudo foi avaliar a condição periodontal eos parâmetros sanguíneos em pacientes alérgicos ao níquel, ummês após remoção dos aparelhos. Noventa e seis pacientesselecionados aleatoriamente foram inicialmente avaliadas. Alergiaao níquel foi diagnosticada usando um teste de contato. Após adeterminação da prevalência de alergia ao níquel, formaram-sedois grupos: 16 pacientes alérgicos (experimental) e 16 nãoalérgicos (controle). Condição periodontal foi diagnosticadaatravés do Índice de Lõe (IG). Parâmetros sanguíneos foramdeterminados por meio de um exame de sangue completo,incluindo a quantificação de níquel e níveis de IgE. Avaliações doestado periodontal foram realizados por um único examinador deforma cega, devidamente calibrado e amostras de sangue foramtomadas depois de nove meses de tratamento e um mês após aremoção dos aparelhos ortodônticos. Análise estatística utilizadafoi testes t pareado e não pareado, Mann-Whitney, Wilcoxon,McNemar e qui-quadrado de tendência linear (p≤0,05). Emcomparação com os valores observados durante o tratamento, onúmero de eosinófilos (p=0,046), basófilos (p=0,001) e monócitos(p=0,002) aumentou significativamente depois da remoção dosaparelhos ortodônticos, ao passo que o número de bastões(p=0,000) diminuiu entre os períodos no grupo alérgico. O númerode linfócitos (p=0,039) aumentou no grupo controle e o número desegmentados (p=0,030) diminuiu. A diminuição dos níveis de IgE(p=0,001) entre os períodos ocorreu no grupo de controle. Níveisde níquel no plasma aumentou após a remoção de aparelhosortodônticos em ambos os grupos (p=0,010; p=0,039). O IGdiminuiu em ambos os grupos. Parâmetros periodontais esanguíneos de pacientes com alergia ao níquel foram semelhantesaos não alérgicos um mês após a remoção dos aparelhos.

Characterization of AQX-1125, a small-molecule SHIP1 activator: Part 2. Efficacy studies in allergic and pulmonary inflammation models in vivo.

BACKGROUND: The efficacy of AQX-1125, a small-molecule SH2-containing inositol-5'-phosphatase 1 (SHIP1) activator and clinical development candidate, is investigated in rodent models of inflammation. EXPERIMENTAL APPROACH: AQX-1125 was administered orally in a mouse model of passive cutaneous anaphylaxis (PCA) and a number of rodent models of respiratory inflammation including: cigarette smoke, LPS and ovalbumin (OVA)-mediated airway inflammation. SHIP1 dependency of the AQX-1125 mechanism of action was investigated by comparing the efficacy in wild-type and SHIP1-deficient mice subjected to an intrapulmonary LPS challenge. RESULTS: AQX-1125 exerted anti-inflammatory effects in all of the models studied. AQX-1125 decreased the PCA response at all doses tested. Using bronchoalveolar lavage (BAL) cell counts as an end point, oral or aerosolized AQX-1125 dose dependently decreased the LPS-mediated pulmonary neutrophilic infiltration at 3-30 mg kg⁻¹ and 0.15-15 µg kg⁻¹ respectively. AQX-1125 suppressed the OVA-mediated airway inflammation at 0.1-10 mg kg⁻¹. In the smoke-induced airway inflammation model, AQX-1125 was tested at 30 mg kg⁻¹ and significantly reduced the neutrophil infiltration of the BAL fluid. AQX-1125 (10 mg kg⁻¹) decreased LPS-induced pulmonary neutrophilia in wild-type mice but not in SHIP1-deficient mice. CONCLUSIONS: The SHIP1 activator, AQX-1125, suppresses leukocyte accumulation and inflammatory mediator release in rodent models of pulmonary inflammation and allergy. As shown in the mouse model of LPS-induced lung inflammation, the efficacy of the compound is dependent on the presence of SHIP1. Pharmacological SHIP1 activation may have clinical potential for the treatment of pulmonary inflammatory diseases.

Indirubin, a purple 3,2- bisindole, inhibited allergic contact dermatitis via regulating T helper (Th)-mediated immune system in DNCB-induced model.

ETHNOPHARMACOLOGICAL RELEVANCE: Indirubin, isolated from Indigo naturalis (Apiaceae) is a purple 3,2- bisindole and a stable isomer of indigo. Although it is known to have anti-inflammatory activities, its mechanism of action has not been elucidated. MATERIALS AND METHODS: Seven-week-old female BALB/c mice were sensitized with 1-chloro-2,4-dinitrobenzene (DNCB) to induce skin inflammation. Hematoxylin and eosin staining was performed to assess epidermal and dermal hyperplasia, which were determined by measuring the thicknesses of the epidermis and dermis, respectively. We also evaluated serum immunoglobulin E (IgE) levels and cytokines production, such as tumor necrosis factor (TNF)-alpha, interleukin (IL)-4, 6 and Interferon (IFN)-gamma. In addition, we investigated nuclear factor (NF)-κB, IκB-α and mitogen-activated protein (MAP) kinase activities for verifying the molecular mechanism of inflammation. RESULTS: Indirubin treatment suppressed skin inflammation in DNCB-exposed mice. The skin lesions were significantly thinner in the Indirubin-treated group than in untreated controls, and the hyperkeratosis disappeared. Indirubin reduced the total serum IgE level and cytokines production. In addition, it normalized NF-κB, IκB-α and MAP kinase expression. CONCLUSIONS: Indirubin might be a useful treatment for allergic contact dermatitis via regulating the co-expression of T helper (Th) 1 and 2 cell-mediated immune responses.

Comparative study of systemic inflammatory responses in psoriasis vulgaris and mild to moderate allergic contact dermatitis.

BACKGROUND: Psoriasis vulgaris (PV) is associated with low-grade systemic inflammation. OBJECTIVE: Cytokines' and growth factors' serum patterns in patients with PV, allergic contact dermatitis (ACD) and healthy subjects were investigated to describe and compare systemic inflammatory responses in these diseases. METHODS: A total of 12 inflammation-sensitive biomarkers were analyzed simultaneously by means of the Evidence Investigator™ biochip technology. RESULTS: In PV, proinflammatory tumor necrosis factor (TNF)-α, interferon (IFN)-γ, interleukins (IL)-1ß, -2, -6, -8, and monocyte chemoattractant protein (MCP)-1 were elevated. In ACD, 2 markers, TNF-α and MCP-1, were increased, and regulatory cytokine IL-10 was decreased. Proinflammatory IL-2 had the strongest correlations with other pro- as well as anti-inflammatory cytokines in PV and ACD, whilst IL-6 correlated positively with the Psoriasis Area and Severity Index. Growth factors' levels correlated with MCP-1, but only in PV. CONCLUSION: Although psoriasis induces a more variegated proinflammatory systemic response, ACD is likewise associated with a systemic increase in inflammatory mediators.

[Analysis of the correlation of prevalence in allergic rhinitis and other allergic diseases].

OBJECTIVE: To obtain the prevalence of allergic rhinitis (AR) in different regions of northern China, to analyze the correlation and interaction between AR and bronchial asthma (BA) or atopic dermatitis (AD), and to provide reference for the prevention and treatment of allergic diseases such as AR. METHODS: To obtain the indexes including age, occupation, atopic physical fitness, smoking, alcohol, lifestyle and so on. To explore the correlation between AR and BA or AD. From April 2007 to May 2010, the serum specific IgE (sIgE) was investigated in different regions (rural areas of Qingxian, Hebei; coastal fishing village of Bohai Bay, Huanghua; area of Wuling Mountain, Chengde; urban areas of Tianjin) by randomly multi-stage and cluster sampling, with total population of 1524. RESULTS: The prevalence of AR, BA and AD were 9.1%, 5.4% and 6.0%. The prevalence of BA and AD were 30.9% and 29.5% in AR patients, but were 2.9% and 3.7% in non-AR, and the differences were of statistical significance (χ(2) values were 192.97 and 148.40, respectively, all P < 0.01). The risk of people with BA suffering from AR was as 8.619 times as those free from BA, the risk of people with AD suffering from AR was as 1.817 times as those free from AD and, the risk of workers suffering from AR was as 2.320 times as farmers in terms of working factor by analysis of Logistic regression for AR and BA, AD, age, occupation, atopic physical fitness and other factors. CONCLUSIONS: The prevalence of AR are correlated with BA and AD. It is greater between BA and AR than AD and AR in the strength of correlation.

Topical application of a phospholipid mixture purified from pig lungs ameliorates 2,4-dinitrofluorobenzene-induced allergic contact dermatitis in BALB/c mice.

This work was designed to assess the pharmacological effectiveness as a novel anti-atopic dermatitis remedy of a phopholipid mixture purified from pig lung tissues, named KT&G101, using the BALB/c mouse model of allergic contact dermatitis. Allergic contact dermatitis was induced by applying 2,4-dinitrofluorobenzene (DNFB) epicutaneously onto the dorsal skins of mice, and KT&G101 was topically applied onto the skin areas with the lesions. The topical application of KT&G101 (0.05 ml of 10 mg/ml and 20 mg/ml KT&G101, twice a day for 15 days) decreased the total IgE level elevated in the sera of mice undergoing allergic contact dermatitis. KT&G101 was also able to decrease the 2,4-dinitrophenyl (DNP)-specific IgE level elevated in the sera of the model mice. It reduced the incidences of scratching behaviors in the mice undergoing DNFB-induced allergic contact dermatitis. It attenuated some histopathological changes, such as pustule, epidermal hyperplasia, dermatitis and fibroplasia, while it could enhance the recovery of epidermis, in the damaged skin tissues within a relatively short period after the topical application of KT&G101. KT&G101 lessened the expression of cytokines mRNAs, such as Th1-specific IL-2, TNF-ß and IFN-γ, and Th2-specific IL-4, in the mouse skin tissues showing the lesions. In brief, it is concluded that KT&G101 alleviates the symptoms involved in induced allergic contact dermatitis in BALB/c mice.

Interaction between filaggrin null mutations and tobacco smoking in relation to asthma.

BACKGROUND: The mechanisms underlying the association between filaggrin (FLG) deficiency and asthma are not known. It has been hypothesized that FLG deficiency leads to enhanced percutaneous exposure to environmental substances that might trigger immune responses. We hypothesized that interactions between FLG deficiency and environmental exposures play a role in asthma development. OBJECTIVE: We sought to investigate possible interactions between FLG null mutations and tobacco smoking in relation to asthma. METHODS: A total of 3471 adults from a general population sample participated in a health examination. Lung function and serum specific IgE levels to inhalant allergens were measured, and information on asthma and smoking was obtained by means of questionnaire. Participants were genotyped for the 2 most common FLG null mutations in white subjects: R501X and 2282del4. Another Danish population was used for replication. RESULTS: The FLG null mutation genotype was significantly associated with a higher prevalence of asthma and decreased FEV(1)/forced vital capacity ratio. In logistic regression analyses with asthma as the outcome, a significant interaction was found between FLG null mutations and smoking status (P = .02). This interaction was confirmed, although it was not statistically significant, in another Danish population study. Interactions between FLG genotype and cumulated smoking exposure were found in relation to asthma (P = .03) and decreased FEV(1)/forced vital capacity ratio (P = .03). A 3-way interaction was found among FLG genotype, smoking, and asthma, suggesting that the FLG-smoking interaction mainly played a role in nonatopic subjects. CONCLUSION: FLG null mutations modified the effects of smoking on the risk of asthma. This finding might have implications for risk stratification of the population.

Effects of palladium nanoparticles on the cytokine release from peripheral blood mononuclear cells of palladium-sensitized women.

OBJECTIVE: To investigate the effects of palladium (Pd) nanoparticles on cytokine release from peripheral blood mononuclear cells (PBMCs) of control or Pd-sensitized nonatopic women. METHODS: TNF-α, IL-5, IL-10 and IFN-γ release and/or expression from PBMCs incubated in presence of 5 to 10 nm Pd nanoparticles or Pd salt (potassium hexachloropalladate) were determined by enzyme-linked immunosorbent assay and reverse transcription-polymerase chain reaction analysis. Transmission electronmicroscopy was performed. RESULTS: In lipopolysaccharide-stimulated PBMCs from controls, Pd salt inhibited IFN-γ and IL-10 release, whereas Pd nanoparticles enhanced IFN-γ release and inhibited TNF-α secretion. In lipopolysaccharide-stimulated PBMCs from Pd-sensitized women showing high IFN-γ release, Pd nanoparticles inhibited TNF-α release and Pd salt IL-10 release. TNF-α and IFN-γ release and messenger RNA expression were correlated. Transmission electronmicroscopy demonstrated uptake of nanoparticles in the endocytic compartment and activation of autophagy. CONCLUSIONS: Palladium ions and nanoparticles exert different effects in vitro on the expression and release of cytokines.

Lesional skin vascular endothelial growth factor levels correlate with clinical severity in patients with cement allergic contact dermatitis.

Allergic contact dermatitis to cement is a delayed-type hypersensitivity reaction in which cytokines interferon-gamma (IEN-y) and vascular endothelial growth factor(VEGF) may be involved in persisting erythema and oedema. VEGF and IFN-gamma levels in serum and skin lesions were measured in 32 Egyptian building workers with chronic allergic contact dermatitis due to occupational exposure to cement and 20 healthy controls. Dermatitis patients had significantly higher levels of serum and lesional skin VEGF and IFN-gamma than controls. A significant positive correlation was found between tissue VEGF and the eczema area and severity index (EASI) score in dermatitis patients (r = 0.86). VEGF and IFN-gamma may play a role in the pathogenesis of cement allergic contact dermatitis.

Serum levels of protein oxidation products in patients with nickel allergy.

Nickel sensitization can not only induce allergic contact dermatitis (ACD), but also can induce an overlapping disease referred to as "systemic nickel allergy syndrome" (SNAS), characterized by urticaria/angioedema and gastrointestinal symptoms correlated to the ingestion of nickel-containing foods. This study was designed to determine if oxidative stress occurs in patients with nickel allergy. Thirty-one female patients (mean age 31.26 + 13.04 years, range 16-64 years) with confirmed nickel CD underwent oral nickel challenge because of clinically suspected SNAS; serum concentrations of protein carbonyl groups (PCGs) and nitrosylated proteins (NPs; biomarkers of oxidative stress) were measured before and after oral nickel challenge as well as in healthy female controls. Twenty-three of these 31 patients were diagnosed with SNAS because they had a positive reaction to the oral nickel challenge, and 8 patients had no reaction and therefore were classified as patients with contact nickel allergy only. Although both nickel-allergic patients and controls presented similar serum levels of PCGs, NP values in nickel-allergic patients appeared higher than in controls and tended to decrease after the challenge; furthermore, serum levels of NPs in patients affected by SNAS were higher (although not significantly) than in patients with nickel ACD only. The involvement of specific biomarkers of oxidative stress such as NPs and the lack of involvement of other biomarkers such as PCGs may help to better understand the alteration of the redox homeostasis occurring in nickel ACD and particularly in SNAS.

Tumour necrotizing factor-alpha promoter and GST-T1 genotype predict skin allergy to chromate in cement workers in Taiwan.

BACKGROUND: Construction workers exposed to cement are known to suffer from occupational contact dermatitis because of chromate sensitization. It is not clear whether certain genotypes are associated with increased susceptibility of chromate sensitization in those workers regularly exposed to cement. OBJECTIVE: The objective of this study was to determine the genotypes predisposing workers to cement-induced contact dermatitis. METHODS: A total of 153 current cement workers who had regular contact with cement were telephone interviewed for skin problems in the past 12 months, work exposure, and personal protection. A dermatologist examined their skin and conducted patch test with common skin allergens. Blood samples were donated for genotypic determination by polymerase chain reaction-based assays for GST-T1, GST-M1 (null/non-null), tumour necrosis factor (TNF) alpha promoter-308G/A, and interleukin (IL) 4-590C/T. RESULT: High percentage of dermatitis was noted in the 153 workers examined, which was correlated with reported skin problems. By patch testing, construction workers had a high-prevalence rate (12%) of sensitivity to chromate. Sensitivity to chromate was significantly associated with TNF alpha promoter-308 heterozygous (GA) as compared with GG genotype (odds ratio 3.9, 95% confidence interval 1.1-13.2), as well as with GST-T1 null genotype (odds ratio 5.5, 95% confidence interval 1.4-36.2), but neither the GST-M1 nor the IL-4 genotypes. CONCLUSION: It is concluded that among workers frequently exposed to cement in Southern Taiwan, those with TNF alpha promoter-308 heterozygous (GA) genotype or GST-T1 null genotype had increased risk of chromate sensitization.