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Involvement of Pollutants in Atopic Dermatitis and Psoriasis

NCT06213688 · Status: NOT_YET_RECRUITING · Phase: NA · Type: INTERVENTIONAL · Enrollment: 64

Last updated 2024-01-19

No results posted yet for this study

Summary

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, levels of AhR activation markers will be compared after stimulation of PBMCs with benzo(a)pyrene.

Conditions

Interventions

OTHER

blood sampling

blood sampling at inclusion

OTHER

urine sampling

urine sampling at inclusion

Sponsors & Collaborators

  • ALPHENYX

    collaborator UNKNOWN

  • Aix Marseille Université

    collaborator OTHER

  • Assistance Publique Hopitaux De Marseille

    lead OTHER

Principal Investigators

  • Richard Marie-Aleth · AP-HM

Study Design

Allocation
NON_RANDOMIZED
Purpose
BASIC_SCIENCE
Masking
NONE
Model
PARALLEL

Eligibility

Min Age
18 Years
Max Age
85 Years
Sex
ALL
Healthy Volunteers
No

Timeline & Regulatory

Start
2024-03-31
Primary Completion
2025-03-31
Completion
2025-03-31

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Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT06213688 on ClinicalTrials.gov