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

2014 ◽  
Vol 142 (10) ◽  
pp. 2195-2206 ◽  
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.

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

2021 ◽  
Author(s):  
Zhihua Hu ◽  
Shaowen Cheng ◽  
Xini Liu ◽  
Lina Xian ◽  
Xinyuan Liang ◽  
...  
Keyword(s):  
Gene Polymorphism ◽  
Publication Bias ◽  
Meta Analysis ◽  
Relevant Literature ◽  
Recessive Model ◽  
Mannose Binding Lectin ◽  
Dominant Model ◽  
Mannose Binding ◽  
Binding Lectin ◽  
Allele Model

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.

scholarly journals Mannose-Binding Lectin is Associated with Thrombosis and Coagulopathy in Critically Ill COVID-19 Patients

2020 ◽  
Vol 120 (12) ◽  
pp. 1720-1724 ◽  
Author(s):  
Michael Hultström ◽  
Robert Frithiof ◽  
Oskar Eriksson ◽  
Barbro Persson ◽  
Miklos Lipcsey ◽  
...  
Keyword(s):  
Critically Ill ◽  
Complement Activation ◽  
Tertiary Hospital ◽  
Mannose Binding Lectin ◽  
Lectin Pathway ◽  
Strongly Correlated ◽  
Increased Risk ◽  
Mannose Binding ◽  
Patients At Risk ◽  
Binding Lectin

AbstractThe ongoing COVID-19 pandemic has caused significant morbidity and mortality worldwide, as well as profound effects on society. COVID-19 patients have an increased risk of thromboembolic (TE) complications, which develop despite pharmacological thromboprophylaxis. The mechanism behind COVID-19-associated coagulopathy remains unclear. Mannose-binding lectin (MBL), a pattern recognition molecule that initiates the lectin pathway of complement activation, has been suggested as a potential amplifier of blood coagulation during thromboinflammation. Here we describe data from a cohort of critically ill COVID-19 patients (n = 65) treated at a tertiary hospital center intensive care unit (ICU). A subset of patients had strongly elevated MBL plasma levels, and activity upon ICU admission, and patients who developed symptomatic TE (14%) had significantly higher MBL levels than patients without TE. MBL was strongly correlated to plasma D-dimer levels, a marker of COVID-19 coagulopathy, but showed no relationship to degree of inflammation or other organ dysfunction. In conclusion, we have identified complement activation through the MBL pathway as a novel amplification mechanism that contributes to pathological thrombosis in critically ill COVID-19 patients. Pharmacological targeting of the MBL pathway could be a novel treatment option for thrombosis in COVID-19. Laboratory testing of MBL levels could be of value for identifying COVID-19 patients at risk for TE events.

Lack of association between Mannose Binding Lectin-2 gene polymorphisms and periodontitis: A meta-analysis

Meta Gene ◽  
2020 ◽  
Vol 26 ◽  
pp. 100757
Author(s):  
Felipe Rodolfo Pereira da Silva ◽  
Alessandro Luiz Araújo Bentes Leal ◽  
Luigi Nibali ◽  
Jae Il Shin ◽  
Marcelo Diniz Carvalho ◽  
...  
Keyword(s):  
Gene Polymorphisms ◽  
Meta Analysis ◽  
Mannose Binding Lectin ◽  
Mannose Binding ◽  
Binding Lectin

scholarly journals Impact of Mannose-Binding Lectin Deficiency on Radiocontrast-Induced Renal Dysfunction

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Michael Osthoff ◽  
Marten Trendelenburg
Keyword(s):  
Endothelial Dysfunction ◽  
Renal Dysfunction ◽  
Serine Proteases ◽  
Vascular Endothelial Cells ◽  
Ischemia Reperfusion ◽  
Mannose Binding Lectin ◽  
Lectin Pathway ◽  
Increased Risk ◽  
Mannose Binding ◽  
Binding Lectin

Contrast-induced nephropathy (CIN) is the third leading cause of acute renal failure in hospitalized patients. Endothelial dysfunction, renal medullary ischemia, and tubular toxicity are regarded as the most important factors in the pathogenesis of CIN. Mannose-binding lectin (MBL), a pattern recognition protein of the lectin pathway of complement, has been found to aggravate and mediate tissue damage during experimental renal ischemia/reperfusion (I/R) injury which was alleviated by inhibition with C1 inhibitor, a potent MBL, and lectin pathway inhibitor. In this paper, we highlight the potential role of MBL in the pathogenesis of human CIN. In experimental I/R models, MBL was previously found to induce tubular cell death independent of the complement system. In addition, after binding to vascular endothelial cells, MBL and its associated serine proteases were able to trigger a proinflammatory reaction and contribute to endothelial dysfunction. In humans, urinary MBL was increased after administration of contrast media and in individuals with CIN. Moreover, individuals with normal/high MBL levels were at increased risk to develop radiocontrast-induced renal dysfunction. Hence, MBL and the lectin pathway seem to be a promising target given that a licensed, powerful, human recombinant inhibitor exits to be added to the scarce armamentarium currently available for prophylaxis of CIN.

scholarly journals Association between Mannose-Binding Lectin Gene Polymorphisms and Hepatitis B Virus Infection: A Meta-Analysis

PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e75371 ◽  
Author(s):  
Hang-di Xu ◽  
Ming-fei Zhao ◽  
Tian-hong Wan ◽  
Guang-zhong Song ◽  
Ji-liang He ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Virus Infection ◽  
Hepatitis B ◽  
Gene Polymorphisms ◽  
Meta Analysis ◽  
Mannose Binding Lectin ◽  
Hepatitis B Virus Infection ◽  
B Virus ◽  
Mannose Binding ◽  
Binding Lectin

scholarly journals Mannose-Binding Lectin Promoter Polymorphisms and Gene Variants in Pulmonary Tuberculosis Patients from Cantabria (Northern Spain)

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
J.-Gonzalo Ocejo-Vinyals ◽  
Lucía Lavín-Alconero ◽  
Pablo Sánchez-Velasco ◽  
M.-Ángeles Guerrero-Alonso ◽  
Fernando Ausín ◽  
...  
Keyword(s):  
Pulmonary Tuberculosis ◽  
Convincing Evidence ◽  
Mannose Binding Lectin ◽  
Gene Variants ◽  
Northern Spain ◽  
Promoter Polymorphisms ◽  
Increased Risk ◽  
Mannose Binding ◽  
Lectin Promoter ◽  
Binding Lectin

Mannose-binding lectin is a central molecule of the innate immune system. Mannose-binding lectin 2 promoter polymorphisms and structural variants have been associated with susceptibility to tuberculosis. However, contradictory results among different populations have been reported, resulting in no convincing evidence of association between mannose-binding lectin 2 and susceptibility to tuberculosis. For this reason, we conducted a study in a well genetically conserved Spanish population in order to shed light on this controversial association. We analysed the six promoter and structural mannose-binding lectin 2 gene variants in 107 patients with pulmonary tuberculosis and 441 healthy controls. Only D variant and HYPD haplotype were significantly more frequents in controls which would indicate that this allele could confer protection against pulmonary tuberculosis, but this difference disappeared after statistical correction. Neither the rest of alleles nor the haplotypes were significantly associated with the disease. These results would indicate that mannose-binding lectin promoter polymorphisms and gene variants would not be associated with an increased risk to pulmonary tuberculosis. Despite the slight trend of the D allele and HYPD haplotype in conferring protection against pulmonary tuberculosis, susceptibility to this disease would probably be due to other genetic factors, at least in our population.

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

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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