Ignite Creation Date:
2024-05-06 @ 3:40 PM
Last Modification Date:
2024-10-26 @ 1:54 PM
Study NCT ID:
NCT04715087
Status:
RECRUITING
Last Update Posted:
2024-05-22
First Post:
2021-01-14
Brief Title:
Staphylococcus Aureus in Atopic Dermatitis Immunopathology
Sponsor:
Hospices Civils de Lyon
Organization:
Hospices Civils de Lyon
Study Overview
Official Title:
Staphylococcus Aureus in Atopic Dermatitis Immunopathology
Status:
RECRUITING
Status Verified Date:
2024-05
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
STADE
Brief Summary:
Atopic Dermatitis AD is a frequent inflammatory skin disease characterized by recurrent eczema It associates geneticepigenetic-induced alterations of epidermal barrier and type-2 inflammationhypersensitivity which may be triggered by different antigens that pass through the altered skin Some studies have reported that environmental pathogens such as house dust mites are able to induce type-2 inflammation through particular activation of innate immunity
Multiple staphylococcal strains are commonly found on the skin of AD patients Interestingly recent findings suggest that S aureus may be a key factor of AD inflammation i 90 of AD patients have S aureus skin colonization on lesional skin ii AD patients with S aureus skin colonization have more increased type-2 inflammatory markers in comparison with AD patients without SA skin colonization iii skin colonization by monoclonal S aureus strains correlate with severe flares and iv S aureus is detected in both epidermis and dermis during AD flares In this study our hypothesis is that S aureus induces AD flares through a type 2 T cell-mediated hypersensitivity against S aureus involving innate and adaptive responses Conversely S epidermidis a commensal strain has a protective effect against S aureus dysbiosis To this end we will characterize in the skin and the blood the immune response induced by cutaneous application of i S aureus isolated from patients with moderate-to-severe AD which will mimic the cutaneous dysbiosis occurring in the natural course of AD ii S aureus toxins without bacteria to evaluate the skin response against those particular proteins iii a laboratory strain of S epidermidis a common well-tolerated skin commensal bacteria iv a mix of S aureus and S epidermidis to evaluate the regulatory effect of S epidermidis on the S aureus-induced AD inflammation
Importantly this characterization will be led in AD patients with alterations of skin barrier compared to healthy volunteers without alterations of skin barrier as controls
Multiple staphylococcal strains are commonly found on the skin of AD patients Interestingly recent findings suggest that S aureus may be a key factor of AD inflammation i 90 of AD patients have S aureus skin colonization on lesional skin ii AD patients with S aureus skin colonization have more increased type-2 inflammatory markers in comparison with AD patients without SA skin colonization iii skin colonization by monoclonal S aureus strains correlate with severe flares and iv S aureus is detected in both epidermis and dermis during AD flares In this study our hypothesis is that S aureus induces AD flares through a type 2 T cell-mediated hypersensitivity against S aureus involving innate and adaptive responses Conversely S epidermidis a commensal strain has a protective effect against S aureus dysbiosis To this end we will characterize in the skin and the blood the immune response induced by cutaneous application of i S aureus isolated from patients with moderate-to-severe AD which will mimic the cutaneous dysbiosis occurring in the natural course of AD ii S aureus toxins without bacteria to evaluate the skin response against those particular proteins iii a laboratory strain of S epidermidis a common well-tolerated skin commensal bacteria iv a mix of S aureus and S epidermidis to evaluate the regulatory effect of S epidermidis on the S aureus-induced AD inflammation
Importantly this characterization will be led in AD patients with alterations of skin barrier compared to healthy volunteers without alterations of skin barrier as controls
Detailed Description:
None
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None
Secondary IDs
| Secondary ID | Type | Domain | Link |
|---|---|---|---|
| 2020-A01547-32 | OTHER | ID-RCB | None |