scholarly journals Impact of MASP2 gene polymorphism and gene-tea drinking interaction on susceptibility to tuberculosis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Zihao Li ◽  
Mian Wang ◽  
Hua Zhong ◽  
Xin Huang ◽  
Xinyin Wu ◽  
...  
Keyword(s):  
Additive Model ◽  
Lectin Pathway ◽  
Control Group ◽  
Single Nucleotide ◽  
Key Enzyme ◽  
Healthy Control ◽  
Tea Drinking ◽  
Mannan Binding Lectin ◽  
The Complement System ◽  
Negative Interactions

AbstractMannan-binding lectin-associated serine protease-2 (MASP-2) has been reported to play an important role as a key enzyme in the lectin pathway of the complement system. The objectives of our study were to determine whether the single-nucleotide polymorphism (SNPs) of MASP2 and the gene-tea drinking interaction were associated with the susceptibility to TB. In total, 503 patients and 494 healthy controls were contained. Three SNPs (rs12142107, rs12711521, and rs7548659) were genotyped. The association between the SNPs and susceptibility to TB were investigated by conducting multivariate unconditional logistic regression analysis. The gene-tea drinking interactions were analyzed by the additive model of marginal structural linear odds models. Both genotype AC + AA at rs12711521 of MASP2 genes and genotype GT + GG at rs7548659 of MASP2 genes were more prevalent in the TB patient group than the healthy control group (OR: 1.423 and 1.439, respectively, P < 0.05). In addition, The relative excess risk of interaction (RERI) between tea drinking and rs12142107, rs12711521, and rs7548659 of MASP2 genes was found to suggest negative interactions, which reached − 0.2311 (95% confidence interval (CI): − 0.4736, − 0.0113), − 0.7080 (95% CI − 1.3998, − 0.0163), and − 0.5140 (95% CI − 0.8988, − 0.1291), respectively (P < 0.05). Our finding indicated that the SNPs (rs12711521 and rs7548659) of MASP2 were associated with the susceptibility to TB. Furthermore, there were negative interactions between tea drinking and rs12142107, rs12711521, and rs75548659 of MASP2 gene, respectively. Our research provides a basis for studying the pathogenesis and prevention of tuberculosis.

scholarly journals Increased Autoreactivity of the Complement-Activating Molecule Mannan-Binding Lectin in a Type 1 Diabetes Model

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Jakob Appel Østergaard ◽  
Marieta Milkova Ruseva ◽  
Talat Habib Malik ◽  
Ingeborg Torp Hoffmann-Petersen ◽  
Matthew Caleb Pickering ◽  
...  
Keyword(s):  
Complement System ◽  
Drug Targets ◽  
Lectin Pathway ◽  
Diabetes Model ◽  
Healthy Control ◽  
End Stage ◽  
Mannan Binding Lectin ◽  
The Complement System ◽  
Binding Lectin ◽  
Immunofluorescence Intensity

Background. Diabetic kidney disease is the leading cause of end-stage renal failure despite intensive treatment of modifiable risk factors. Identification of new drug targets is therefore of paramount importance. The complement system is emerging as a potential new target. The lectin pathway of the complement system, initiated by the carbohydrate-recognition molecule mannan-binding lectin (MBL), is linked to poor kidney prognosis in diabetes. We hypothesized that MBL activates complement upon binding within the diabetic glomerulus.Methods. We investigated this by comparing complement deposition and activation in kidneys from streptozotocin-induced diabetic mice and healthy control mice.Results. After 20 weeks of diabetes, glomerular deposition of MBL was significantly increased. Diabetic animals had 2.0-fold higher (95% CI 1.6–2.5) immunofluorescence intensity from anti-MBL antibodies compared with controls (P<0.001). Diabetes and control groups did not differ in glomerular immunofluorescence intensity obtained by antibodies against complement factors C4, C3, and C9. However, the circulating complement activation product C3a was increased in diabetes as compared to control mice (P=0.04).Conclusion. 20 weeks of diabetes increased MBL autoreactivity in the kidney and circulating C3a concentration. Together with previous findings, these results indicate direct effects of MBL within the kidney in diabetes.

scholarly journals Diabetes Is Associated with Increased Autoreactivity of Mannan-Binding Lectin

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Esben Axelgaard ◽  
Jakob Appel Østergaard ◽  
Steffen Thiel ◽  
Troels Krarup Hansen
Keyword(s):  
Diabetic Nephropathy ◽  
Complement System ◽  
Knockout Mice ◽  
Ex Vivo ◽  
Lectin Pathway ◽  
Urine Albumin ◽  
Mannan Binding Lectin ◽  
The Complement System ◽  
Binding Lectin

Mannan-binding lectin (MBL) has been reported to be involved in the pathophysiology of diabetic nephropathy. MBL is a pattern-recognition molecule of the innate immune system that initiates the lectin pathway of the complement system upon recognition of evolutionary conserved pathogen-associated molecular patterns or to altered self-tissue. Our group have previously shown direct effects of MBL on diabetes-induced kidney damage, and we hypothesized that MBL may cause autoactivation of the complement system via binding to neoepitopes induced by hyperglycemia. In the present study, we induced diabetes in MBL knockout mice and in wild type C57BL/6J mice by low-dose streptozotocin injection and measured blood glucose and urine albumin-to-creatinine ratio to monitor development of diabetes. After 24 weeks, fluorescently labelled recombinant MBL was injected intravenously in diabetic MBL knockout mice after which the distribution was investigated using in vivo fluorescence imaging. Mice were subjected to in vivo and ex vivo imaging 24 hours after injection. MBL was found to accumulate in the kidneys of diabetic mice as compared to healthy control mice (p<0.0001). These findings support the hypothesis of a significant role of MBL and the complement system in the pathophysiology of diabetic nephropathy.

scholarly journals Human IgA Activates the Complement System Via the Mannan-Binding Lectin Pathway

2001 ◽  
Vol 167 (5) ◽  
pp. 2861-2868 ◽  
Author(s):  
Anja Roos ◽  
Lee H. Bouwman ◽  
Daniëlle J. van Gijlswijk-Janssen ◽  
Maria C. Faber-Krol ◽  
Gregory L. Stahl ◽  
...  
Keyword(s):  
Complement System ◽  
Lectin Pathway ◽  
Mannan Binding Lectin ◽  
The Complement System ◽  
Binding Lectin

scholarly journals Meta-Analysis of Polymyositis and Dermatomyositis Microarray Data Reveals Novel Genetic Biomarkers

Genes ◽  
2019 ◽  
Vol 10 (11) ◽  
pp. 864 ◽  
Author(s):  
Jaeseung Song ◽  
Daeun Kim ◽  
Juyeon Hong ◽  
Go Woon Kim ◽  
Junghyun Jung ◽  
...  
Keyword(s):  
Drug Targets ◽  
Meta Analysis ◽  
Control Group ◽  
Nucleotide Polymorphisms ◽  
Immune Disorder ◽  
Single Nucleotide ◽  
Unfolded Protein ◽  
Healthy Control ◽  
Protein Response ◽  
Potential Drug Targets

Polymyositis (PM) and dermatomyositis (DM) are both classified as idiopathic inflammatory myopathies. They share a few common characteristics such as inflammation and muscle weakness. Previous studies have indicated that these diseases present aspects of an auto-immune disorder; however, their exact pathogenesis is still unclear. In this study, three gene expression datasets (PM: 7, DM: 50, Control: 13) available in public databases were used to conduct meta-analysis. We then conducted expression quantitative trait loci analysis to detect the variant sites that may contribute to the pathogenesis of PM and DM. Six-hundred differentially expressed genes were identified in the meta-analysis (false discovery rate (FDR) < 0.01), among which 317 genes were up-regulated and 283 were down-regulated in the disease group compared with those in the healthy control group. The up-regulated genes were significantly enriched in interferon-signaling pathways in protein secretion, and/or in unfolded-protein response. We detected 10 single nucleotide polymorphisms (SNPs) which could potentially play key roles in driving the PM and DM. Along with previously reported genes, we identified 4 novel genes and 10 SNP-variant regions which could be used as candidates for potential drug targets or biomarkers for PM and DM.

scholarly journals Associations of BAFF rs2893321 polymorphisms with myasthenia gravis susceptibility

2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Hui Deng ◽  
Jianjian Wang ◽  
Xiaotong Kong ◽  
Huixue Zhang ◽  
Tianfeng Wang ◽  
...  
Keyword(s):  
Myasthenia Gravis ◽  
B Lymphocyte ◽  
Chinese Han Population ◽  
Control Group ◽  
B Cell Differentiation ◽  
Chinese Han ◽  
Single Nucleotide ◽  
Han Population ◽  
Gender And Age ◽  
Healthy Control

Abstract Background Myasthenia gravis (MG) is an autoimmune diseases characterized by fatigue and weakness of skeletal muscles. B-lymphocyte-activating factor (BAFF), an essential factor for B cell differentiation and development, is important in the progression of MG. The current study aimed to investigate the association between single nucleotide polymorphism rs2893321 in BAFF with MG susceptibility in Chinese Han population. Methods One hundred forty-nine patients with MG and 148 healthy controls were recruited. Using improved multiple ligase detection reaction technology, the polymorphisms of rs2893321 between groups and among MG subgroups have been compared. Results A significant differences between the MG group and the healthy control group was observed. Additionally, rs2893321 was found to be associated with gender and age in patients with MG. Conclusion Genetic variations of rs2893321 in BAFF might be associated with susceptibility to MG in the Chinese Han population.

scholarly journals Genetic association study between TAB2 polymorphisms and noise-induced-hearing-loss in a Han Chinese population

PLoS ONE ◽  
2021 ◽  
Vol 16 (5) ◽  
pp. e0251090
Author(s):  
Guangzhi Yang ◽  
Boshen Wang ◽  
Dawei Sun ◽  
Huimin Wang ◽  
Mengyao Chen ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Association Study ◽  
Genetic Association ◽  
Genetic Association Study ◽  
Control Group ◽  
Case Group ◽  
Noise Induced Hearing Loss ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Healthy Control

Noise-induced-hearing-loss(NIHL) is a common occupational disease caused by various environmental and biological factors. To investigate the association between TAB2 and the susceptibility of NIHL of people exposed to occupational environments, a genetic association study was performed on selected companies with 588 cases and 537 healthy control subjects. Five selected single nucleotide polymorphisms (SNPs) in TAB2,incoluding rs2744434, rs521845, rs652921, rs7896, rs9485372, were genotyped after a collection of DNA samples. Evident differences in participants between the case group and the control group reveals the result that people with the TAB2 has a high probability of getting NIHL. The results show that rs521845 is deeply associated with the risk of NIHL and is available for the diagnosis in the future.

The -11377C > G Adiponectin Gene Polymorphism Alters the Adiponectin Concentration and the Susceptibility to Type 2 Diabetes in Thais

2010 ◽  
Vol 80 (3) ◽  
pp. 216-224 ◽  
Author(s):  
Kanjana Suriyaprom ◽  
Benjaluck Phonrat ◽  
Pisit Namjuntra ◽  
Talabporn Harnroongroj ◽  
Rungsunn Tungtrongchitr
Keyword(s):  
Type 2 Diabetes ◽  
Waist Circumference ◽  
Gene Polymorphism ◽  
Gene Polymorphisms ◽  
Control Group ◽  
Adiponectin Gene ◽  
Adiponectin Concentration ◽  
Single Nucleotide ◽  
Healthy Control

The aims of this study were first to detect the levels of adiponectin, insulin, albumin, glucose, alanine aminotransferase (ALT), lipids, homeostasis model assessment for insulin resistance (HOMA-IR), and anthropometric variables in type 2 diabetes mellitus (T2DM) as well as healthy control groups, and to determine whether two adiponectin gene polymorphisms, at the position -11377C > G as well as +45T > G, are associated with serum levels of adiponectin and other variables; then to search for the association between these two single nucleotide polymorphisms (SNPs) of the adiponectin gene and T2DM. We investigated 93 T2DM patients and 90 healthy volunteers. Compared with the healthy control group, the T2DM group had significantly lower adiponectin levels. Waist circumference, total cholesterol, ALT, glucose, insulin, and HOMA-IR scores were significantly higher in the T2DM group than in the control group. The polymorphism of the adiponectin gene at position -11377C > G among type 2 diabetes subjects showed that the adiponectin concentration was significantly lower in CG/GG genotypes (6.2 μg/mL) than the CC genotype (7.8 μg/mL), whereas SNP +45T > G was not associated with adiponectin levels. Adiponectin gene polymorphisms at position -11377C > G and +45T > G were significantly more frequent in type 2 diabetes patients than in the control group (p = 0.022; p = 0.045, respectively). However, multivariate logistic regression analysis showed that the strong impact on T2DM was found for -11377C > G gene polymorphism (p = 0.023) and waist circumference (p < 0.001). Therefore, the single nucleotide polymorphism of -11377C > G in adiponectin promoter region has impact on the lower adiponectin concentrations, and may influence susceptibility to T2DM in Thais.

Vitamin D Treatment in Patients with Hashimoto’s Thyroiditis may Decrease the Development of Hypothyroidism

2016 ◽  
Vol 86 (1-2) ◽  
pp. 9-17 ◽  
Author(s):  
Bekir Ucan ◽  
Mustafa Sahin ◽  
Muyesser Sayki Arslan ◽  
Nujen Colak Bozkurt ◽  
Muhammed Kizilgul ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Hashimoto’S Thyroiditis ◽  
Healthy Control Group ◽  
Hashimoto's Thyroiditis ◽  
Control Group ◽  
Endocrine Society ◽  
Thyroid Autoantibody ◽  
Healthy Control ◽  
The Mean

Abstract.The relationship between Hashimoto’s thyroiditis and vitamin D has been demonstrated in several studies. The aim of the present study was to evaluate vitamin D concentrations in patients with Hashimoto’s thyroiditis, the effect of vitamin D therapy on the course of disease, and to determine changes in thyroid autoantibody status and cardiovascular risk after vitamin D therapy. We included 75 patients with Hashimoto’s thyroiditis and 43 healthy individuals. Vitamin D deficiency is defined as a 25-hydroxy vitamin D (25(OH)D3) concentration less than 20ng/mL. Vitamin D deficient patients were given 50.000 units of 25(OH)D3 weekly for eight weeks in accordance with the Endocrine Society guidelines. All evaluations were repeated after 2 months of treatment. Patients with Hashimoto’s thyroiditis had significantly lower vitamin D concentrations compared with the controls (9.37±0.69 ng/mL vs 11.95±1.01 ng/mL, p < 0.05, respectively). Thyroid autoantibodies were significantly decreased by vitamin D replacement treatment in patients with euthyroid Hashimoto’s thyroiditis. Also, HDL cholesterol concentrations improved in the euthyroid Hashimoto group after treatment. The mean free thyroxine (fT4) concentrations were 0.89±0.02 ng/dL in patients with Hashimoto’s thyroiditis and 1.07±0.03 ng/dL in the healthy control group (p < 0.001). The mean thyroid volumes were 7.71±0.44 mL in patients with Hashimoto’s thyroiditis and 5.46±0.63 mL in the healthy control group (p < 0.01). Vitamin D deficiency is frequent in Hashimoto’s thyroiditis and treatment of patients with this condition with Vitamin D may slow down the course of development of hypothyroidism and also decrease cardiovascular risks in these patients. Vitamin D measurement and replacement may be critical in these patients.

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