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 Role of mannose binding lectin gene variants on its protein levels and macrophage phagocytosis with liveMycobacterium tuberculosisin pulmonary tuberculosis

2006 ◽  
Vol 46 (3) ◽  
pp. 433-437 ◽  
Author(s):  
Paramasivam Selvaraj ◽  
Mohideen S. Jawahar ◽  
Dhanushkodi N. Rajeswari ◽  
Kalichamy Alagarasu ◽  
Mohankumar Vidyarani ◽  
...  
Keyword(s):  
Pulmonary Tuberculosis ◽  
Mannose Binding Lectin ◽  
Gene Variants ◽  
Lectin Gene ◽  
Protein Levels ◽  
Macrophage Phagocytosis ◽  
Mannose Binding ◽  
Binding Lectin

Mannose-binding lectin promoter and structural gene variants in sarcoidosis

2000 ◽  
Vol 30 (6) ◽  
pp. 549-552 ◽  
Author(s):  
Foley ◽  
Mullighan ◽  
McGrath ◽  
Pantelidis ◽  
Marshall ◽  
...  
Keyword(s):  
Structural Gene ◽  
Mannose Binding Lectin ◽  
Gene Variants ◽  
Mannose Binding ◽  
Lectin Promoter ◽  
Binding Lectin

P962 Mannose-binding lectin promoter gene variants in Korean patient with bacteraemia

2007 ◽  
Vol 29 ◽  
pp. S253
Author(s):  
Y.S. Park ◽  
J.Y. Choi ◽  
S.Y. Shin ◽  
M.S. Kim ◽  
Y.H. Kim ◽  
...  
Keyword(s):  
Mannose Binding Lectin ◽  
Gene Variants ◽  
Korean Patient ◽  
Mannose Binding ◽  
Promoter Gene ◽  
Lectin Promoter ◽  
Binding Lectin

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.

Transcription efficiency of different chicken mannose-binding lectin promoter alleles

2014 ◽  
Vol 66 (12) ◽  
pp. 737-742 ◽  
Author(s):  
R. M. Kjærup ◽  
T. S. Dalgaard ◽  
L. R. Norup ◽  
R. M. Goto ◽  
M. M. Miller ◽  
...  
Keyword(s):  
Mannose Binding Lectin ◽  
Mannose Binding ◽  
Transcription Efficiency ◽  
Lectin Promoter ◽  
Binding Lectin

scholarly journals Evaluation of Mannose Binding Lectin Gene Variants in Pediatric Influenza Virus-Related Critical Illness

2019 ◽  
Vol 10 ◽  
Author(s):  
Emily R. Levy ◽  
Wai-Ki Yip ◽  
Michael Super ◽  
Jill M. Ferdinands ◽  
Anushay J. Mistry ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Critical Illness ◽  
Mannose Binding Lectin ◽  
Gene Variants ◽  
Lectin Gene ◽  
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.

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