scholarly journals Genetic markers of inflammation may not contribute to metabolic traits in Mexican children

PeerJ ◽  
2016 ◽  
Vol 4 ◽  
pp. e2090 ◽  
Author(s):  
Neeti Vashi ◽  
Carolina Stryjecki ◽  
Jesus Peralta-Romero ◽  
Fernando Suarez ◽  
Jaime Gomez-Zamudio ◽  
...  
Keyword(s):  
Leptin Receptor ◽  
Interleukin 10 ◽  
P Value ◽  
Low Grade ◽  
Nucleotide Polymorphisms ◽  
Necrosis Factor Alpha ◽  
Metabolic Complications ◽  
Metabolic Traits ◽  
Mexican Children ◽  
Markers Of Inflammation

Background:Low-grade chronic inflammation is a common feature of obesity and its cardio-metabolic complications. However, little is known about a possible causal role of inflammation in metabolic disorders. Mexico is among the countries with the highest obesity rates in the world and the admixed Mexican population is a relevant sample due to high levels of genetic diversity.Methods:Here, we studied 1,462 Mexican children recruited from Mexico City. Six genetic variants in five inflammation-related genes were genotyped: rs1137101 (leptin receptor (LEPR)), rs7305618 (hepatocyte nuclear factor 1 alpha (HNF1A)), rs1800629 (tumor necrosis factor alpha (TNFA)), rs1800896, rs1800871 (interleukin-10 (IL-10)), rs1862513 (resistin (RETN)). Ten continuous and eight binary traits were assessed. Linear and logistic regression models were used adjusting for age, sex, and recruitment centre.Results:We found that one SNP displayed a nominal evidence of association with a continuous trait: rs1800871 (IL-10) with LDL (beta = −0.068 ± 1.006, P = 0.01). Subsequently, we found one nominal association with a binary trait: rs7305618 (HNF1A) with family history of hypertension (odds-ratio = 1.389 [1.054–1.829], P = 0.02). However, no P-value passed the Bonferroni correction for multiple testing.Discussion:Our data in a Mexican children population are consistent with previous reports in European adults in failing to demonstrate an association between inflammation-associated single nucleotide polymorphisms (SNPs) and metabolic traits.

scholarly journals Relationship of Markers of Inflammation, Infection and Endothelial Function to Mortality and Severity of Coagulopathy in Patients with Sepsis-Associated DIC

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 2495-2495
Author(s):  
Debra Hoppensteadt ◽  
Amanda Walborn ◽  
Matthew T. Rondina ◽  
Jawed Fareed
Keyword(s):  
Endothelial Function ◽  
Protein C ◽  
Conflicts Of Interest ◽  
Interleukin 10 ◽  
Response To Treatment ◽  
Necrosis Factor Alpha ◽  
Multiple Systems ◽  
Markers Of Inflammation ◽  
Prediction Of Mortality ◽  
Pai 1

Abstract Background: Sepsis-associated disseminated intravascular coagulation (DIC) is a complex clinical scenario involving derangement of many processes, including hemostasis. Assessment of markers of these other aspects of disease, including inflammation, immunity, endothelial function, and endogenous anticoagulants may provide insight into DIC pathophysiology and lead to improved methods for assessment of patient condition and response to treatment. This study was designed to measure biomarkers representative of multiple systems involved in DIC development in a cohort of patients with sepsis and DIC and determine the association of these biomarkers with disease severity and mortality. Materials and Methods: Citrated plasma samples were prospectively collected from 102 patients with sepsis and suspected DIC at ICU admission (day 0) and again serially on ICU days 4 and 8 under an IRB approved protocol. DIC score was determined using the ISTH scoring algorithm (e.g. platelet count, PT/INR, fibrinogen, and D-Dimer). Plasma from healthy individuals was purchased from a commercial laboratory (George King Biomedical, Overland, KS). . CD 40 Ligand (CD40L), Plasminogen inhibitor 1 ( PAI-1), nucleosomes, Procalcitonun (PCT), Microparicle Tissue Factor (MP-TF), and Prothrombin Fragment 1.2 (F1.2) were measured using commercially available ELISA kits. Protein C activity was measured using a clot-based assay. Interleukin 6 (IL-6), Interleukin 8 (IL-8), Interleukin 10 (IL-10) , Tumor Necrosis Factor Alpha (TNFα) , Monocyte Chemoattractant protein 1 (MCP-1) were measured using a biochip technology. Results: Significant differences in levels of Protein C (p=0.009), PCT (p=0.0005), IL-6 (p=0.019), IL-8 (p= 0.015), and PAI-1 (p=0.015) were observed between survivors and non-survivors (Table 1). Significant variation of Protein C (p=0.002), nucleosomes (p=0.05), PCT (P<0.001), IL-6 (p=0.001), IL-8 (p=0.003), IL-10 (p=0.011), TNFα (p=0.021), and MCP-1 (p=0.21), were observed based on severity of DIC score. Conclusion: Markers from multiple systems perturbed in DIC were associated with mortality suggesting that while these systems may not be routinely evaluated in the course of patient care, dysfunction of these system contribute significantly to mortality. In addition, numerous inflammatory cytokines showed an association with DIC score. This study suggests that the measurement of additional markers in sepsis-associated DIC may be of value in the prediction of mortality and may be helpful in guiding treatment for these patients. Disclosures No relevant conflicts of interest to declare.

Influence of Polymorphisms of Pro-Inflammatory (IL-12, TNFa and LTa) and Anti-Inflammatory Factors (IL-10 and CTLA4) in Autoimmune Hemolytic Anemia.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3751-3751
Author(s):  
Maria S. Figueiredo ◽  
Leandro S. D’Abronzo ◽  
Melca M. Oliveira ◽  
Juliana L. Dreyfuss ◽  
Jose Orlando Bordin
Keyword(s):  
Hemolytic Anemia ◽  
Patient Group ◽  
Autoimmune Hemolytic Anemia ◽  
Interleukin 10 ◽  
Inflammatory Factors ◽  
Interleukin 12 ◽  
Control Group ◽  
Nucleotide Polymorphisms ◽  
Necrosis Factor Alpha ◽  
Anti Inflammatory

Abstract The Autoimmune Hemolytic Anemia (AIHA) is caused by the destruction of antibody-coated red blood cells, but mechanisms that initiate the production of autoantibodies remains unclear. It had been suggest that decreased production of Th1-type cytokines and production of autoantibodies in AIHA can be secondary to the imbalance between anti- and pro-inflammatory factors. Moreover, the presence of single nucleotide polymorphisms (SNPs) showed association with different production of immunoregulatory factors which may modulate the disease expression in AIHA. OBJECTIVES: To determine the importance of SNPs of pro- and anti-inflammatory factors in the development of AIHA. PATIENTS: We studied 17 patients with AIHA who has been followed in the Hematology and Blood Transfusion Unit at the Federal University of Sao Paulo (UNIFESP/EPM), Brazil. The control group was composed by 40 healthy volunteer blood donors. METHODS: After DNA extraction from peripheral blood samples, the frequency of the SNPs was determinate by PCR-RFLP in patients and healthy individuals. The following SNPs were analyzed: Interleukin 12: IL-12 1188 (A/C), Tumor Necrosis Factor alpha: TNFa-308 (G/A), and Lymphotoxin alpha: Lta +252 (A/G); Interleukin 10: IL-10-592 (C/A), and Cytotoxic T-lymphocyte associated protein 4: CTLA4 exon 1 49 (A/G). RESULTS: The patient group was composed predominantly by female individuals (14 or 82%) and the median of age was 56 years old (18 to 76 years). The frequency observed for each allele studied in the patient group was: allele A of IL-12 = 0.82; allele G of FNTa = 0.85; allele A of Lta = 0.68; allele C of IL-10 = 0.82; allele G of CTLA4 = 0.59. No differences in allele frequency were found between patient and control groups. CONCLUSIONS: Our results suggest that these polymorphisms appear not to contribute for the development of the AIHA.

scholarly journals Susceptibility and Severity of Viral Infections in Obesity: Lessons from Influenza to COVID-19. Does Leptin Play a Role?

2021 ◽  
Vol 22 (6) ◽  
pp. 3183
Author(s):  
Valeria Guglielmi ◽  
Luca Colangeli ◽  
Monica D’Adamo ◽  
Paolo Sbraccia
Keyword(s):  
Immune System ◽  
Infectious Diseases ◽  
Leptin Receptor ◽  
Viral Infections ◽  
Immune Surveillance ◽  
Adaptive Immune System ◽  
Leptin Resistance ◽  
Future Research ◽  
Low Grade ◽  
Metabolic Complications

The recent pandemic Sars-CoV2 infection and studies on previous influenza epidemic have drawn attention to the association between the obesity and infectious diseases susceptibility and worse outcome. Metabolic complications, nutritional aspects, physical inactivity, and a chronic unbalance in the hormonal and adipocytokine microenvironment are major determinants in the severity of viral infections in obesity. By these pleiotropic mechanisms obesity impairs immune surveillance and the higher leptin concentrations produced by adipose tissue and that characterize obesity substantially contribute to such immune response dysregulation. Indeed, leptin not only controls energy balance and body weight, but also plays a regulatory role in the interplay between energy metabolism and immune system. Since leptin receptor is expressed throughout the immune system, leptin may exert effects on cells of both innate and adaptive immune system. Chronic inflammatory states due to metabolic (i.e., obesity) as well as infectious diseases increase leptin concentrations and consequently lead to leptin resistance further fueling inflammation. Multiple factors, including inflammation and ER stress, contribute to leptin resistance. Thus, if leptin is recognized as one of the adipokines responsible for the low grade inflammation found in obesity, on the other hand, impairments of leptin signaling due to leptin resistance appear to blunt the immunologic effects of leptin and possibly contribute to impaired vaccine-induced immune responses. However, many aspects concerning leptin interactions with inflammation and immune system as well as the therapeutical approaches to overcome leptin resistance and reduced vaccine effectiveness in obesity remain a challenge for future research.

Impact of polymorphisms in genes involved in autoimmune disease on inhibitor development in Chinese patients with haemophilia A

2012 ◽  
Vol 107 (01) ◽  
pp. 30-36 ◽  
Author(s):  
Yeling Lu ◽  
Qiulan Ding ◽  
Jing Dai ◽  
Hongli Wang ◽  
Xuefeng Wang
Keyword(s):  
Cytotoxic T Lymphocyte ◽  
Interleukin 10 ◽  
Chinese Patients ◽  
Haemophilia A ◽  
Nucleotide Polymorphisms ◽  
Necrosis Factor Alpha ◽  
Ca Repeat ◽  
Inhibitor Development ◽  
Tnf Α ◽  
Genes Encoding

SummaryOne of the most severe and important complication in the treatment of haemophilia A (HA) patients is the formation of inhibitors. The mechanism that leads to factor (F)VIII inhibitor formation is complicated. Both genetic and environmental factors have been mentioned to play decisive roles. Recently, polymorphisms in the genes encoding interleukin-10 (IL-10), tumour necrosis factor-alpha (TNF-α), cytotoxic T-lymphocyte antigen-4 (CTLA-4), have been suggested to be contributing determinants of the inhibitor risk. In order to investigate the influence of the single nucleotide polymorphisms (SNPs) in the genes encoding for cytokines to the inhibitors development in Chinese HA patients, we genotyped 10 SNPs with high heterozygote rates in Chinese and a CA repeat microsatellite at the gene loci IL-10 as well in a separate, unrelated case-controlled cohort of 122 affected HA patients; 63 with inhibitors and 59 without inhibitors. The particular SNPs included in this study were as follows: –592C/A and –819C/T in IL-10, –590C/T in IL-4, –318C/T and 49A/G in CTLA-4, –827C/T in TNF-α, –1112C/T and 2044G/A in IL-13, 874A/T in interferon (IFN)-γ and –295T/C in IL-16. Our results demonstrated that –819T and –592A alleles in IL-10 were observed more frequently in patients with inhibitors. This indicated that –819C/T and –592A/C in IL-10 may influence the inhibitors development in HA patients. Furthermore, we concluded that the haplotype in IL-10 (TA, CA, CC at positions –819 and –582, respectively) may predispose FVIII inhibitor development in HA patients. In conclusion, the data reported in our study clearly highlight the participation of IL-10 in inhibitors formation in Chinese HA patients.

scholarly journals Effects and Responsiveness of a Multicomponent Intervention on Body Composition, Physical Fitness and Leptin in Overweight/Obese Adolescents

2021 ◽  
Vol 18 (14) ◽  
pp. 7267
Author(s):  
Leticia Borfe ◽  
Caroline Brand ◽  
Letícia Schneiders ◽  
Jorge Mota ◽  
Claudia Cavaglieri ◽  
...  
Keyword(s):  
Body Composition ◽  
Physical Fitness ◽  
Intervention Group ◽  
Interleukin 10 ◽  
Control Group ◽  
Post Intervention ◽  
Necrosis Factor Alpha ◽  
Obese Adolescents ◽  
Quasi Experimental ◽  
Multicomponent Program

Physical exercise reduces the biochemical markers of obesity, but the effects of multicomponent interventions on these markers should be explored. The present study aimed to elucidate how overweight/obese adolescents respond to a multicomponent program approach on body composition, physical fitness, and inflammatory markers, using a quasi-experimental study with 33 overweight/obesity adolescents (control group (CG) = 16; intervention group (IG) = 17). The intervention consisted of 24 weeks with physical exercises and nutritional and psychological guidance. Both groups were evaluated at the pre/post-intervention moments on body mass index (BMI); body fat (%Fat); waist circumference (WC); waist/hip ratio (WHR); waist-to-height ratio (WHtR), cardiorespiratory fitness (CRF); abdominal strength, flexibility; leptin; interleukin 6; interleukin 10; and tumor necrosis factor-alpha. Mixed-analysis of variance and generalized estimation equations were used for statistical analysis. There was an interaction effect between groups and time on %Fat (p = 0.002), WC (p = 0.023), WHR (p < 0.001), WHtR (p = 0.035), CRF (p = 0.050), and leptin (p = 0.026). Adolescents were classified as 82.4% responders for %Fat, 70.6% for WC, 88.2% for WHR, and 70.6% for CRF. Further, there was an association between changes in %Fat (p = 0.033), WC (p = 0.032), and WHR (p = 0.033) between responders and non-responders with CRF in the IG. There was a positive effect on body composition, physical fitness, and leptin. In addition, reductions in body composition parameters were explained by CRF improvements.

scholarly journals Sex Differences in Circadian Clock Genes and Myocardial Infarction Susceptibility

2021 ◽  
Vol 8 (5) ◽  
pp. 53
Author(s):  
Ivana Škrlec ◽  
Jasminka Talapko ◽  
Martina Juzbašić ◽  
Robert Steiner
Keyword(s):  
Myocardial Infarction ◽  
Cardiovascular Disease ◽  
Circadian Rhythm ◽  
Single Nucleotide Polymorphisms ◽  
Clock Genes ◽  
P Value ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Biological Sex ◽  
Significant Difference

The growing body of evidence shows a significant difference in the circadian rhythm of cardiovascular disease based on biological sex. The incidence of cardiovascular disease varies between women and men. Additionally, biological sex is vital for the timely application of therapy—chronotherapy, which benefits both sexes. This study aimed to examine the potential difference of single nucleotide polymorphisms (SNPs) of the circadian rhythm genes ARNTL, CLOCK, CRY2 and PER2 in women and men with myocardial infarction. A cross-sectional study was conducted, including 200 patients with myocardial infarction. Altogether, ten single nucleotide polymorphisms in the ARNTL, CLOCK, CRY2 and PER2 genes were analyzed. The Chi-square test yielded statistically significant differences in CLOCK gene rs11932595 polymorphism in a recessive genotype model between women and men with a p-value of 0.03 and an odds ratio 2.66, and a corresponding 95% confidence interval of 1.07 to 6.66. Other analyzed polymorphisms of the circadian rhythm genes ARNTL, CRY2, and PER2 did not significantly differ between the sexes. According to the study’s current results, the CLOCK gene’s genetic variability might affect myocardial infarction concerning biological sex.

scholarly journals Common and Novel Markers for Measuring Inflammation and Oxidative Stress Ex Vivo in Research and Clinical Practice—Which to Use Regarding Disease Outcomes?

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 414
Author(s):  
Alain Menzel ◽  
Hanen Samouda ◽  
Francois Dohet ◽  
Suva Loap ◽  
Mohammed S. Ellulu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Clinical Practice ◽  
Acute Phase Proteins ◽  
Ex Vivo ◽  
Chronic Obstructive ◽  
Low Grade ◽  
Obstructive Pulmonary Disease ◽  
Amyloid A ◽  
Non Invasive ◽  
Markers Of Inflammation

Many chronic conditions such as cancer, chronic obstructive pulmonary disease, type-2 diabetes, obesity, peripheral/coronary artery disease and auto-immune diseases are associated with low-grade inflammation. Closely related to inflammation is oxidative stress (OS), which can be either causal or secondary to inflammation. While a low level of OS is physiological, chronically increased OS is deleterious. Therefore, valid biomarkers of these signalling pathways may enable detection and following progression of OS/inflammation as well as to evaluate treatment efficacy. Such biomarkers should be stable and obtainable through non-invasive methods and their determination should be affordable and easy. The most frequently used inflammatory markers include acute-phase proteins, essentially CRP, serum amyloid A, fibrinogen and procalcitonin, and cytokines, predominantly TNFα, interleukins 1β, 6, 8, 10 and 12 and their receptors and IFNγ. Some cytokines appear to be disease-specific. Conversely, OS—being ubiquitous—and its biomarkers appear less disease or tissue-specific. These include lipid peroxidation products, e.g., F2-isoprostanes and malondialdehyde, DNA breakdown products (e.g., 8-OH-dG), protein adducts (e.g., carbonylated proteins), or antioxidant status. More novel markers include also –omics related ones, as well as non-invasive, questionnaire-based measures, such as the dietary inflammatory-index (DII), but their link to biological responses may be variable. Nevertheless, many of these markers have been clearly related to a number of diseases. However, their use in clinical practice is often limited, due to lacking analytical or clinical validation, or technical challenges. In this review, we strive to highlight frequently employed and useful markers of inflammation-related OS, including novel promising markers.

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