ClinicalTrials.gov
public full text
Public Domain
Involvement of Pollutants in Atopic Dermatitis and Psoriasis
Introduction Pollution is a significant public health issue. Research has shown a positive correlation between air pollution and chronic inflammatory dermatoses, including psoriasis and eczema. The incidence of these diseases has been steadily increasing since the beginning of industrialization. The mechanism behind this association involves the activation of the aromatic hydrocarbon receptor (AhR). The aryl hydrocarbon receptor (AhR) plays a role in regulating the balance between T helper 17 (TH17) and regulatory T cells (TREG), as well as in generating oxidative stress and producing pro-inflammatory cytokines. Studies in cultured keratinocytes have shown that a non-competitive antagonist that modulates AhR activity can reduce cutaneous inflammatory processes induced by polycyclic aromatic hydrocarbons (PAHs). Objectives: It has been suggested that activation of the AhR by PAHs and dioxins may be related to the pathogenesis of atopic dermatitis and psoriasis. The main objective is to compare the levels of AhR pathway activation markers between cases and controls. Secondary objectives include correlating environmental exposure to AhR ligands with disease severity in patients. Finally, we will compare the expression of inflammatory and AhR activation markers in cultured peripheral blood mononuclear cells (PBMCs) after in vitro stimulation with benzo(a)pyrene. Material and methods: The study will measure exposure to pollutants by determining blood dioxins and urinary PAH metabolites. Pro-inflammatory cytokines IL1β, TNFα, IL23, IL17 and IFNγ and Malondialdehyde (MDA) serum concentrations will be measured by ELISA. The TREG and TH17 lymphocyte population ratio will be evaluated by flow cytometry on isolated PBMCs. Additionally, the level of expression of CYP 1A1 and 1B1, pollutant-metabolizing enzymes induced by AhR, will be assessed on isolated PBMCs. The expression levels of the AhR and NfkB active fractions will be determined by immunofluorescence. Subsequently,
Conceptio Open Archive
Analyze & explore related research in Conceptio
Connect this record directly into your research workflow or AI agent. Explore citations across open repositories, query full text, and export structured proof bundles.
This document is indexed with metadata only: full text is not available in the archive for this record. Open the official source ↗
Related documents
- The Role of Filaggrin and FADS Genes on the Concentrations of PUFA Towards Its Effect on Atopic Dermatitis in Infants#1140506
- Observational Evaluation of Atopic Dermatitis in Pediatric Patients#1096390
- Cytokine gene polymorphisms and atopic disease in two European cohorts (ECRHS-Basel and SAPALDIA)#402104
- Trends in the Epidemiology and Treatment of Atopic Dermatitis in the United Kingdom (UK)#1046631
- Treatment and Medical Care of Patients With Moderate-to-severe Atopic Dermatitis - TREATswitzerland#912562
Record · ID 825326
Retrieved via Conceptio: every document is proof-bundled with source, license, and retrieval metadata.
Retrieved via Conceptio: every document is proof-bundled with source, license, and retrieval metadata.
Bring this data into your agent: Connect via MCP or API · 20 free credits to start · no card required
Read the Docs → · View CLI source on GitHub · Conceptio Open Knowledge Archive
Read the Docs → · View CLI source on GitHub · Conceptio Open Knowledge Archive