Mannose-binding lectin gene polymorphism and the susceptibility of sepsis: A meta-analysis

Abstract Objective To assess the association between the Mannose-binding lectin (MBL) gene polymorphism and the susceptibility to sepsis using a meta-analysis.Methods The publications were searched on PubMed, Embase, and Web of Science databases up to December 1, 2019 for relevant literature. Results A total of 32 studies (21 adult and 11 pediatric studies) were selected for analysis. Overall, in the three models of MBL +54 A/B gene polymorphisms, namely the dominant model BB + AB vs. AA (p = 0.03), the recessive model BB vs. AB + AA (p < 0.00001), and the allele model B vs. A (p = 0.04), MBL +54A/B was significantly related to the risk of sepsis. In the adult group, the MBL A/O gene polymorphism was associated with the risk of sepsis in the dominant model AO + OO vs. AA (p = 0.006) as well as in the allele model O vs. A (p = 0.04). The MBL +54A/B gene polymorphism was significantly related to the risk of sepsis in the recessive model and, therefore, may increase the risk of sepsis. In the pediatric group, no polymorphic loci were significantly associated with sepsis in any of the three models. The results of the publication bias test demonstrated no publication bias in an unadjusted estimate of the relationship between MBL A/O and -211Y/X gene polymorphism and sepsis.

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Genetic association between mannose-binding lectin polymorphisms and viral hepatitis: a meta-analysis

Pathogens and Disease ◽

10.1093/femspd/ftz035 ◽

2019 ◽

Vol 77 (7) ◽

Author(s):

Chunhua Qie ◽

Yamin Liu ◽

Ping Ma ◽

Hongzhang Wu

Keyword(s):

Viral Hepatitis ◽

Genetic Association ◽

Association Studies ◽

Meta Analysis ◽

Mannose Binding Lectin ◽

Dominant Model ◽

Subgroup Analyses ◽

Mannose Binding ◽

Exon 1 ◽

Binding Lectin

ABSTRACT Some previous genetic association studies have tried to investigate potential associations between mannose-binding lectin (MBL) polymorphisms and viral hepatitis. However, the results of those studies were not consistent. Therefore, we performed the current meta-analysis to explore associations between MBL polymorphisms and viral hepatitis in a large pooled population. A systematic literature research of PubMed, Web of Science, Embase and CNKI was performed to identify eligible studies for pooled analyses. We used Review Manager version 5.3.3 to conduct statistical analyses. In total, 27 studies were included for analysis (4840 cases and 5729 controls). The pooled analyses showed that MBL promoter (-211C/G, dominant model: P = 0.0002, I2 = 40%; over-dominant model: P = 0.0001, I2 = 22%) and exon 1 (codon 52, 54 and 57, dominant model: P = 0.04, I2 = 49%; allele model: P = 0.01, I2 = 48%) polymorphisms were both significantly associated with viral hepatitis in the overall population. Further subgroup analyses revealed similarly significant findings for MBL promoter polymorphism in HBV and HCV, but no positive results were detected in subgroup analyses for MBL exon 1 polymorphism. These results suggested that MBL promoter and exon 1 polymorphisms could be used to identify individuals at higher susceptibility to HBV and HCV.

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Mannose-binding lectin polymorphisms and the risk of sepsis: evidence from a meta-analysis

Epidemiology and Infection ◽

10.1017/s0950268813003361 ◽

2014 ◽

Vol 142 (10) ◽

pp. 2195-2206 ◽

Cited By ~ 8

Author(s):

A.-Q. ZHANG ◽

C.-L. YUE ◽

W. PAN ◽

J.-W. GAO ◽

L. ZENG ◽

...

Keyword(s):

Subgroup Analysis ◽

Meta Analysis ◽

Recessive Model ◽

Mannose Binding Lectin ◽

Large Sample Size ◽

Increased Risk ◽

Confounding Variables ◽

Mannose Binding ◽

Binding Lectin ◽

Related Mortality

SUMMARYSeveral studies have evaluated the association between mannose-binding lectin (MBL) polymorphisms and sepsis. However, the results are inconclusive and conflicting. To better understand the roles of MBL polymorphisms in sepsis, we conducted a comprehensive meta-analysis. All relevant studies were searched from PubMed, EMBASE and Web of Knowledge databases, with the last report up to 7 May 2013. Twenty-nine studies addressing four MBL polymorphisms (–550G/C, –221G/C, structure variant A/O, Gly54Asp) were analysed for susceptibility to sepsis and one study for sepsis-related mortality. Overall, significant associations between structure variant A/O and susceptibility to sepsis were observed for AO + OO vs. AA [odds ratio (OR) 1·27, 95% confidence interval (CI) 1·05–1·52, P = 0·01] and O vs. A (OR 1·19, 95% CI 1·02–1·40, P = 0·03). In subgroup analysis based on age group, increased risk was found in the paediatric group in the dominant model (OR 1·72, 95% CI 1·16–2·56, P = 0·007). Moreover, there was a slight association between the +54A/B polymorphism and susceptibility to sepsis in Caucasians (recessive model: OR 10·64, 95% CI 1·24–91·65, P = 0·03). However, no association was observed for –550G/C and –221G/C polymorphisms both overall and in subgroup analysis. For sepsis-related mortality, only one study suggested AO/OO was associated with in-hospital mortality in pneumococcal sepsis patients after controlling for confounding variables. Our meta-analysis indicated that MBL structure variants might be associated with susceptibility to sepsis but further studies with a large sample size should be conducted to confirm these findings.

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