Association between egg and staphylococcal superantigen IgE sensitizations in atopic dermatitis.
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ABSTRACT:
SUBMITTER: Ong PY
PROVIDER: S-EPMC5554375 | biostudies-other | 2014 Jul-Aug
REPOSITORIES: biostudies-other
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Project description:BackgroundAtopic dermatitis (AD) is a complex chronic inflammatory disease where allergens can act as specific triggering factors.AimTo characterize the specificities of IgE-reactivity in patients with AD to a broad panel of exogenous allergens including microbial and human antigens.MethodologyAdult patients with AD were grouped according to the SCORAD index, into severe (n = 53) and moderate AD (n = 126). As controls 43 patients were included with seborrhoeic eczema and 97 individuals without history of allergy or skin diseases. Specific IgE reactivity was assessed in plasma using Phadiatop®, ImmunoCap™, micro-arrayed allergens, dot-blotted recombinant Malassezia sympodialis allergens, and immune-blotted microbial and human proteins.ResultsIgE reactivity was detected in 92% of patients with severe and 83% of patients with moderate AD. Sensitization to cat allergens occurred most frequently, followed by sensitization to birch pollen, grass pollen, and to the skin commensal yeast M. sympodialis. Patients with severe AD showed a significantly higher frequency of IgE reactivity to allergens like cat (rFel d 1) and house dust mite (rDer p 4 and 10), to Staphylococcus aureus, M. sympodialis, and to human antigens. In contrast, there were no significant differences in the frequencies of IgE reactivity to the grass pollen allergens rPhl p 1, 2, 5b, and 6 between the two AD groups. Furthermore the IgE reactivity profile of patients with severe AD was more spread towards several different allergen molecules as compared to patients with moderate AD.ConclusionWe have revealed a hitherto unknown difference regarding the molecular sensitization profile in patients with severe and moderate AD. Molecular profiling towards allergen components may provide a basis for future investigations aiming to explore the environmental, genetic and epigenetic factors which could be responsible for the different appearance and severity of disease phenotypes in AD.
| S-EPMC4881900 | biostudies-literature
Project description:Atopic dermatitis (AD) is a chronic, relapsing, and inflammatory skin disorder. It is characterized by an inappropriate skin barrier function, allergen sensitization, and recurrent skin infections. Resistin is an adipokine expressed mainly in macrophages and monocytes; it has a role in the inflammatory process and is associated with multiple inflammatory human diseases; however, only few studies linked resistin to atopic dermatitis. This study tested the association between G>A (rs3745367) and C>T (rs3219177) single nucleotide polymorphisms (SNPs) of the RETN gene with atopic dermatitis. In addition, it explored the relationship between serum resistin protein and atopic dermatitis. To achieve objectives of this study, 162 atopic dermatitis patients and 161 healthy participants were recruited in the study. A significant association was detected between rs3745367 and atopic dermatitis with age and gender specificity (p < 0.05), while no significant association between rs3219177 and atopic dermatitis was found (p > 0.05). For the serum resistin levels, a significant decrease was indicated in atopic dermatitis patients compared to healthy subjects (p < 0.05). In conclusion, rs3745367 may play a gender and age-specific role in atopic dermatitis. In addition, the significant decrease in the resistin protein level confirmed this association.
| S-EPMC6023010 | biostudies-literature
Project description:Atopic dermatitis (AD) may affect academic performance through multiple pathways, including poor concentration associated with itching, sleep deprivation, or adverse effects of medications. Because educational attainment is associated with health and well-being, any association with a prevalent condition such as AD is of major importance. To examine whether a childhood diagnosis of AD is associated with lower educational attainment. This population-based cohort study used linked routine health care data from January 1, 1977, to June 30, 2017 (end of registry follow-up), in Denmark. The study population included all children born in Denmark on June 30, 1987, or earlier with an inpatient or outpatient hospital clinic diagnosis of AD recorded before their 13th birthday (baseline) and a comparison cohort of children from the general population matched by birth year and sex. A secondary analysis included exposure-discordant full siblings as a comparison cohort to account for familial factors. Data were analyzed from September 11, 2019, to January 21, 2021. Hospital-diagnosed AD. Estimated probability or risk of not attaining specific educational levels (lower secondary, upper secondary, and higher) by 30 years of age among children with AD compared with children in the matched general population cohort. Corresponding risk ratios (RRs) were computed using Poisson regression that was conditioned on matched sets and adjusted for age. The sibling analysis was conditioned on family and adjusted for sex and age. The study included a total of 61 153 children, 5927 in the AD cohort (3341 male [56.4%]) and 55 226 from the general population (31 182 male [56.5%]). Compared with matched children from the general population, children with AD were at increased risk of not attaining lower secondary education (150 of 5927 [2.5%] vs 924 of 55 226 [1.7%]; adjusted RR, 1.50; 95% CI, 1.26-1.78) and upper secondary education (1141 of 5777 [19.8%] vs 8690 of 52 899 [16.4%]; RR, 1.16; 95% CI, 1.09-1.24), but not higher education (2406 of 4636 [51.9%] vs 18 785 of 35 408 [53.1%]; RR, 0.95; 95% CI, 0.91-1.00). The absolute differences in probability were less than 3.5%. The comparison of 3259 children with AD and 4046 of their full siblings yielded estimates that were less pronounced than those in the main analysis (adjusted RR for lower secondary education, 1.29 [95% CI, 0.92-1.82]; adjusted RR for upper secondary education, 1.05 [95% CI, 0.93-1.18]; adjusted RR for higher education, 0.94 [95% CI, 0.87-1.02]). This population-based cohort study found that hospital-diagnosed AD was associated with reduced educational attainment, but the clinical importance was uncertain owing to small absolute differences and possible confounding by familial factors in this study. Future studies should examine for replicability in other populations and variation by AD phenotype.
| S-EPMC8047754 | biostudies-literature
Project description:Atopic dermatitis (AD) is a chronic skin condition with intense pruritus, eczema, and dry skin. The recurrent intense pruritus and numerous complications in patients with AD can profoundly affect their quality of life. Obesity is one of its comorbidities that has been confirmed to be the hazard factor of AD and also worsen its severity. Nevertheless, the specific mechanisms that explain the connection between obesity and AD remain incompletely recognized. Recent studies have built hopes on various adipokines to explain this connection. Adipokines, which are disturbed by an obese state, may lead to immune system imbalances in people with AD and promote the development of the disease. This review focuses on the abnormal expression patterns of adipokines in patients with AD and their potential regulatory molecular mechanisms associated with AD. The connection between AD and obesity is elucidated through the involvement of adipokines. This conduces to the in-depth exploration of AD pathogenesis and provides a new perspective to develop therapeutic targets.
| S-EPMC10804547 | biostudies-literature
Project description:Background & objectivesAtopic diseases, including atopic dermatitis (AD), allergy and asthma, are complex diseases resulting from the effect of multiple genetic and interacting environmental factors on their pathophysiology. The genetic basis is incompletely understood; however, recent studies have shown an association between loss-of-function variants of the filaggrin gene (FLG) and atopic dermatitis. The aim of this study was to determine whether FLG variants can serve as a predictor for atopic diseases in Korean individuals.MethodsA total of 648 subjects were genotyped for the FLG P478S (rs11584340, C/T base change) polymorphism (322 patients and 326 controls). Serum levels of free fatty acids (FFA) and IgE were later stratified to determine the effects of the FLG polymorphism on AD.ResultsA significant difference in genotype frequency was found between AD patients and controls in the FLG P478S polymorphism. The FLG P478S T allele carrier (TT+TC) was associated with AD risk (odds ratio = 1.877, 95% confidence interval 1.089 to 3.234). In addition, the P478S T allele was related to high levels of FFA in AD patients (471.79 ± 298.96 vs. 333.54 ± 175.82 μg eq/l, P <0.05).Interpretation & conclusionsThe results of the present study suggest that the FLG P478S polymorphism alone and combined with other factors influences FFA levels and increases the susceptibility to AD.
| S-EPMC3978983 | biostudies-literature
Project description:Atopic dermatitis (AD) is a chronic recurrent inflammatory skin disease. There are a lot of evidences on the importance of vitamin D and house dust mite (HDM) allergens in the etiology and course of AD. The objectives of this study are to evaluate the relation between vitamin D3 level and house dust mites (HDM) Dermatophagoidspecies sensitization in pathogenesis of atopic dermatitis. Cross-sectional design study was conducted on 50 atopic dermatitis patients. Blood analysis were done to determine level of vitamin D3, total IgE by fluorescent immunoassay & specific IgE for HDM (d1, d2) & other inhalant allergens by ELISA test. There was significant high negative correlation with the specific IgE for HDM (r?=??-0. 62, p?<?0.001) and vitamin D3. & there was non-significant minimal negative correlation with the specific IgE and other inhalant allergens (r?=?-?0.10, p?>?0.05). There was a statistically significant relation between level of vitamin D3 and atopic dermatitis severity and sensitization to HDM and other allergens.
| S-EPMC7710713 | biostudies-literature
Project description:PURPOSE:Atopic dermatitis (AD) is a common and chronic inflammatory skin disease affecting up to 20% of children and 3% of adults worldwide. Although previous reports including genome-wide association study (GWAS) approaches have identified several risk factors that appear to be associated with AD development, replication studies are lacking. In our current study, we replicated the associations between candidate susceptibility loci and AD. METHODS:A total of 885 Korean subjects (425 AD patients and 460 unaffected controls) were genotyped for 17 single nucleotide polymorphisms (SNPs) from previous GWASs and meta-analyses of AD and from immune-related genes. RESULTS:Several SNPs showed significant associations with AD in the case-control analysis (minimum P=0.005 at rs17389644), suggesting that these polymorphisms may be related to this disease. In addition, several SNPs showed significant signals (minimum P=0.004 at rs6473227) in severe AD compared to unaffected controls. In additional linear regression analysis, a few genotypes appeared to have potential effects on the SCORing AD (SCORAD) values (minimum P=0.003 at rs13361382 on TMEM232) and immunoglobulin E (IgE) levels (minimum P<0.0001 at rs4713555 near HLA-DRB1 and HLA-DQA1) in AD patients. CONCLUSIONS:Our replication and extended study provide additional supporting information on the genetic associations (especially, variants in TMEM232 and nearby to IL21 and HLA-DRB1/HLA-DQA1) related to AD, its clinical severity and IgE involvement.
| S-EPMC6021591 | biostudies-literature
Project description:Protein tyrosine phosphatase-22 (PTPN22) gene encodes lymphoid-specific tyrosine phosphatase (Lyp), an inhibitor of T cell activation. A polymorphism of the PTPN22 gene has been found to be associated with chronic urticaria (CU). We investigated the associations between PTPN22 gene polymorphisms and CU characteristics, including serum specific IgE antibodies response to toxic shock syndrome toxin-1 (TSST-1) and staphylococcal enterotoxin A (SEA). CU patients (n=409) and normal healthy controls (n=388) were enrolled in the present study. Serum specific IgE to TSST-1 and SEA were measured by ImmunoCAP®. Five PTPN22 single nucleotide polymorphisms, -1123G>C, 1858C>T, 13145A>G, 14943C>T, and 20628A>G, were genotyped. There were no significant differences in genotype or haplotype frequencies of these polymorphisms between the 2 groups. CU patients carrying the GG genotype at 20628A>G (P=0.035) or haplotype 3 [GGG] (P=0.047) had a significantly higher prevalence of serum specific IgE to TSST-1 compared to non-carriers. Similarly, CT/TT genotype at 14943C>T had a significantly higher prevalence of serum specific IgE to SEA (P=0.045). The findings suggest that the PTPN22 gene polymorphisms at 20628A>G and 14943C>T may enhance serum specific IgE responses to TSST-1 and SEA, which may contribute to CU pathogenesis.
| S-EPMC4397370 | biostudies-literature
Project description:The skin microbiota of atopic dermatitis (AD) patients is characterized by increased Staphylococcus aureus colonization, which exacerbates disease symptoms and has been linked to reduced bacterial diversity. Skin bacterial communities in AD patients have mostly been described at family and genus levels, while species-level characterization has been limited. In this study, we investigated the role of the bacteria belonging to the Staphylococcus genus using targeted sequencing of the tuf gene with genus-specific primers. We compared staphylococcal communities on lesional and non-lesional skin of AD patients, as well as AD patients with healthy controls, and determined the absolute abundance of bacteria present at each site. We observed that the staphylococcal community, bacterial alpha diversity, and bacterial densities were similar on lesional and non-lesional skin, whereas AD severity was associated with significant changes in staphylococcal composition. Increased S. aureus, Staphylococcus capitis, and Staphylococcus lugdunensis abundances were correlated with increased severity. Conversely, Staphylococcus hominis abundance was negatively correlated with severity. Furthermore, S. hominis relative abundance was reduced on AD skin compared to healthy skin. In conclusion, various staphylococcal species appear to be important for skin health.
| S-EPMC7921937 | biostudies-literature
Project description:Atopic dermatitis (AD) is a multifactorial, chronic relapsing disease associated with genetic and environmental factors. Among skin microbes, Staphylococcus aureus and Staphylococcus epidermidis are associated with AD, but how genetic variability and staphylococcal strains shape the disease remains unclear. We investigated the skin microbiome of an AD cohort (n = 54) as part of a prospective natural history study using shotgun metagenomic and whole genome sequencing, which we analyzed alongside publicly available data (n = 473). AD status and global geographical regions exhibited associations with strains and genomic loci of S. aureus and S. epidermidis. In addition, antibiotic prescribing patterns and within-household transmission between siblings shaped colonizing strains. Comparative genomics determined that S. aureus AD strains were enriched in virulence factors, whereas S. epidermidis AD strains varied in genes involved in interspecies interactions and metabolism. In both species, staphylococcal interspecies genetic transfer shaped gene content. These findings reflect the staphylococcal genomic diversity and dynamics associated with AD.
| S-EPMC10151067 | biostudies-literature