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Role of Mannose-binding Lectin and Association with Microbial Sensitization in a Cohort of Patients with Atopic Dermatitis

Atopic dermatitis is a relapsing inflammatory skin condition, in which bacteria, fungi and viruses may colonize the skin and aggravate the condition. Mannose-binding lectin is part of the innate immune system. Polymorphism in the mannose-binding lectin gene can result in deficiency of mannose-bindin...

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Autores principales: BELFRAGE, Emma, JINNESTÅL, Camilla L., JÖNSEN, Andreas, BENGTSSON, Anders, ÅKESSON, Anna, SCHMIDTCHEN, Artur, SONESSON, Andreas
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medical Journals Sweden, on behalf of the Society for Publication of Acta Dermato-Venereologica 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10134062/
https://www.ncbi.nlm.nih.gov/pubmed/36994777
http://dx.doi.org/10.2340/actadv.v103.2405
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author BELFRAGE, Emma
JINNESTÅL, Camilla L.
JÖNSEN, Andreas
BENGTSSON, Anders
ÅKESSON, Anna
SCHMIDTCHEN, Artur
SONESSON, Andreas
author_facet BELFRAGE, Emma
JINNESTÅL, Camilla L.
JÖNSEN, Andreas
BENGTSSON, Anders
ÅKESSON, Anna
SCHMIDTCHEN, Artur
SONESSON, Andreas
author_sort BELFRAGE, Emma
collection PubMed
description Atopic dermatitis is a relapsing inflammatory skin condition, in which bacteria, fungi and viruses may colonize the skin and aggravate the condition. Mannose-binding lectin is part of the innate immune system. Polymorphism in the mannose-binding lectin gene can result in deficiency of mannose-binding lectin, which may affect defence against microbes. The aim of this study was to investigate whether polymorphisms in the mannose-binding lectin gene affect the extent of sensitization to common skin microbes, the skin barrier function, or the severity of the disease in a cohort of patients with atopic dermatitis. Genetic testing of mannose-binding lectin polymorphism was performed in 60 patients with atopic dermatitis. The disease severity, skin barrier function, and serum levels of specific immunoglobulin E against skin microbes were measured. In patients with low mannose-binding lectin genotype (group 1) 6 of 8 (75%) were sensitized to Candida albicans, compared to 14 of 22 (63.6%) patients with intermediate mannose-binding genotype (group 2) and 10 of 30 (33.3%) patients with high mannose-binding genotype (group 3). Group 1 (low mannose-binding lectin) was more likely to be sensitized to Candida albicans compared with group 3 (high mannose-binding lectin) (odds ratio 6.34, p-value 0.045). In this cohort of patients with atopic dermatitis, mannose-binding lectin deficiency was associated with increased sensitization to Candida albicans.
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spelling pubmed-101340622023-04-28 Role of Mannose-binding Lectin and Association with Microbial Sensitization in a Cohort of Patients with Atopic Dermatitis BELFRAGE, Emma JINNESTÅL, Camilla L. JÖNSEN, Andreas BENGTSSON, Anders ÅKESSON, Anna SCHMIDTCHEN, Artur SONESSON, Andreas Acta Derm Venereol Original Report Atopic dermatitis is a relapsing inflammatory skin condition, in which bacteria, fungi and viruses may colonize the skin and aggravate the condition. Mannose-binding lectin is part of the innate immune system. Polymorphism in the mannose-binding lectin gene can result in deficiency of mannose-binding lectin, which may affect defence against microbes. The aim of this study was to investigate whether polymorphisms in the mannose-binding lectin gene affect the extent of sensitization to common skin microbes, the skin barrier function, or the severity of the disease in a cohort of patients with atopic dermatitis. Genetic testing of mannose-binding lectin polymorphism was performed in 60 patients with atopic dermatitis. The disease severity, skin barrier function, and serum levels of specific immunoglobulin E against skin microbes were measured. In patients with low mannose-binding lectin genotype (group 1) 6 of 8 (75%) were sensitized to Candida albicans, compared to 14 of 22 (63.6%) patients with intermediate mannose-binding genotype (group 2) and 10 of 30 (33.3%) patients with high mannose-binding genotype (group 3). Group 1 (low mannose-binding lectin) was more likely to be sensitized to Candida albicans compared with group 3 (high mannose-binding lectin) (odds ratio 6.34, p-value 0.045). In this cohort of patients with atopic dermatitis, mannose-binding lectin deficiency was associated with increased sensitization to Candida albicans. Medical Journals Sweden, on behalf of the Society for Publication of Acta Dermato-Venereologica 2023-03-30 /pmc/articles/PMC10134062/ /pubmed/36994777 http://dx.doi.org/10.2340/actadv.v103.2405 Text en © Published by Medical Journals Sweden, on behalf of the Foundation for Rehabilitation Information https://creativecommons.org/licenses/by-nc/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (https://creativecommons.org/licenses/by-nc/4.0/)
spellingShingle Original Report
BELFRAGE, Emma
JINNESTÅL, Camilla L.
JÖNSEN, Andreas
BENGTSSON, Anders
ÅKESSON, Anna
SCHMIDTCHEN, Artur
SONESSON, Andreas
Role of Mannose-binding Lectin and Association with Microbial Sensitization in a Cohort of Patients with Atopic Dermatitis
title Role of Mannose-binding Lectin and Association with Microbial Sensitization in a Cohort of Patients with Atopic Dermatitis
title_full Role of Mannose-binding Lectin and Association with Microbial Sensitization in a Cohort of Patients with Atopic Dermatitis
title_fullStr Role of Mannose-binding Lectin and Association with Microbial Sensitization in a Cohort of Patients with Atopic Dermatitis
title_full_unstemmed Role of Mannose-binding Lectin and Association with Microbial Sensitization in a Cohort of Patients with Atopic Dermatitis
title_short Role of Mannose-binding Lectin and Association with Microbial Sensitization in a Cohort of Patients with Atopic Dermatitis
title_sort role of mannose-binding lectin and association with microbial sensitization in a cohort of patients with atopic dermatitis
topic Original Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10134062/
https://www.ncbi.nlm.nih.gov/pubmed/36994777
http://dx.doi.org/10.2340/actadv.v103.2405
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