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Association between dectin-1 gene single nucleotide polymorphisms and fungal infection: a systemic review and meta-analysis

Objectives: To investigate the association between dectin-1 gene single nucleotide polymorphisms (SNPs) and susceptibility to fungal infection (FI). Methods: Databases were searched electronically and manually to identify case–control studies concerning dectin-1 SNPs and FI, which were published up...

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Autores principales: Zhou, Peiru, Xie, Yufei, Yan, Zhimin, Liu, Xiaosong, Hua, Hong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6851518/
https://www.ncbi.nlm.nih.gov/pubmed/31696220
http://dx.doi.org/10.1042/BSR20191519
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author Zhou, Peiru
Xie, Yufei
Yan, Zhimin
Liu, Xiaosong
Hua, Hong
author_facet Zhou, Peiru
Xie, Yufei
Yan, Zhimin
Liu, Xiaosong
Hua, Hong
author_sort Zhou, Peiru
collection PubMed
description Objectives: To investigate the association between dectin-1 gene single nucleotide polymorphisms (SNPs) and susceptibility to fungal infection (FI). Methods: Databases were searched electronically and manually to identify case–control studies concerning dectin-1 SNPs and FI, which were published up to 12 November 2018. The Newcastle–Ottawa Quality Assessment Scale was used to determine the study quality and bias. The SNP frequencies of the B (the variant or minor allele) and A (the wild or major allele) alleles of the dectin-1 gene in both cases and controls were analyzed with regard to FI susceptibility. Results: Eight high-quality studies were included in the review. Systemic review of the included studies demonstrated that dectin-1 SNPs rs3901533 and rs7309123 might be associated with susceptibility to invasive pulmonary aspergillosis infection; moreover, rs16910527 SNP can possibly increase the susceptibility to oropharyngeal candidiasis in HIV-positive patients. The meta-analysis identified significant associations between dectin-1 SNPs and overall FI risk in the homozygote model (pooled odds ratio (OR) 1.77, P=0.04). When classified by subtypes, significant associations were also found for deep FI in the homozygote model (pooled OR 2.46, P=0.01) and the recessive model (pooled OR 2.85, P=0.002). There appeared to be no significant association between dectin-1 SNPs and superficial FI. Conclusion: Systemic review of the included studies suggested that dectin-1 SNPs rs3901533, rs7309123, and rs16910527 might play a role in FI susceptibility. The meta-analysis provided convincing evidence that dectin-1 SNPs might have an important role in FI susceptibility, especially for deep FI.
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spelling pubmed-68515182019-11-19 Association between dectin-1 gene single nucleotide polymorphisms and fungal infection: a systemic review and meta-analysis Zhou, Peiru Xie, Yufei Yan, Zhimin Liu, Xiaosong Hua, Hong Biosci Rep Host-Microbe Interactions Objectives: To investigate the association between dectin-1 gene single nucleotide polymorphisms (SNPs) and susceptibility to fungal infection (FI). Methods: Databases were searched electronically and manually to identify case–control studies concerning dectin-1 SNPs and FI, which were published up to 12 November 2018. The Newcastle–Ottawa Quality Assessment Scale was used to determine the study quality and bias. The SNP frequencies of the B (the variant or minor allele) and A (the wild or major allele) alleles of the dectin-1 gene in both cases and controls were analyzed with regard to FI susceptibility. Results: Eight high-quality studies were included in the review. Systemic review of the included studies demonstrated that dectin-1 SNPs rs3901533 and rs7309123 might be associated with susceptibility to invasive pulmonary aspergillosis infection; moreover, rs16910527 SNP can possibly increase the susceptibility to oropharyngeal candidiasis in HIV-positive patients. The meta-analysis identified significant associations between dectin-1 SNPs and overall FI risk in the homozygote model (pooled odds ratio (OR) 1.77, P=0.04). When classified by subtypes, significant associations were also found for deep FI in the homozygote model (pooled OR 2.46, P=0.01) and the recessive model (pooled OR 2.85, P=0.002). There appeared to be no significant association between dectin-1 SNPs and superficial FI. Conclusion: Systemic review of the included studies suggested that dectin-1 SNPs rs3901533, rs7309123, and rs16910527 might play a role in FI susceptibility. The meta-analysis provided convincing evidence that dectin-1 SNPs might have an important role in FI susceptibility, especially for deep FI. Portland Press Ltd. 2019-11-13 /pmc/articles/PMC6851518/ /pubmed/31696220 http://dx.doi.org/10.1042/BSR20191519 Text en © 2019 The Author(s). https://creativecommons.org/licenses/by/4.0/ This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY).
spellingShingle Host-Microbe Interactions
Zhou, Peiru
Xie, Yufei
Yan, Zhimin
Liu, Xiaosong
Hua, Hong
Association between dectin-1 gene single nucleotide polymorphisms and fungal infection: a systemic review and meta-analysis
title Association between dectin-1 gene single nucleotide polymorphisms and fungal infection: a systemic review and meta-analysis
title_full Association between dectin-1 gene single nucleotide polymorphisms and fungal infection: a systemic review and meta-analysis
title_fullStr Association between dectin-1 gene single nucleotide polymorphisms and fungal infection: a systemic review and meta-analysis
title_full_unstemmed Association between dectin-1 gene single nucleotide polymorphisms and fungal infection: a systemic review and meta-analysis
title_short Association between dectin-1 gene single nucleotide polymorphisms and fungal infection: a systemic review and meta-analysis
title_sort association between dectin-1 gene single nucleotide polymorphisms and fungal infection: a systemic review and meta-analysis
topic Host-Microbe Interactions
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6851518/
https://www.ncbi.nlm.nih.gov/pubmed/31696220
http://dx.doi.org/10.1042/BSR20191519
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