Interleukin-10 Gene Polymorphisms Research Articles

Interleukin-10 Gene Polymorphisms Modulate the Risk of Infertility in Chlamydia trachomatis Positive Kurdish Women in Erbil Province.

There is evident inter-individual variability in women's responses to Chlamydial infections and reproductive tract problems. Women's genetic variations within the Interleukin-10 (IL-10) gene have been linked to variances in response to Chlamydia trachomatis infection. This study was aimed to demonstrate the profound association of IL-10 with infertility and demonstrate the role of IL-10 (-592 C/A rs1800872) and (-1082 A>G rs1800896) single nucleotide polymorphism (SNPs) gene in the susceptibility and severity of a C. trachomatis infection. In this evaluation study, serum IL-10 concentration was measured in 134 women diagnosed with infertility and 50 healthy volunteers by enzyme-linked immunosorbent assay (ELISA). The tetra-amplification refractory mutation system-PCR (T-ARMS-PCR) analysis was performed to detect the genotyping of the rs1800872 and rs1800896 SNPs genes. Both female groups were positive for anti-chlamydial IgM antibody, but the intensity of response differed between cases. At the same time, the incidence of genital C. trachomatis by PCR was 46.2% in infertile women. The serum concentration of IL10 was lower in infertile women than healthy participants and higher in infertile C. trachomatis -positive women compared to infertile C. trachomatis-negative in all groups except endometriosis (Endo) infertility. In rs1800872, the CA genotype and C allele are associated with an increased risk for infertility, except in polycystic ovarian syndrome (PCOS), which is an A allele. In the case of rs1800896, the AG genotype and G allele show a greater risk for infertility. Our results confirmed that rs1800872 and rs1800896 gene polymorphisms were associated with an increased risk of C. trachomatis infection.

Interleukin-18 Gene Polymorphisms and Rheumatoid Arthritis Susceptibility: An Umbrella Review of Meta-Analyses.

This study systematically analyzes the association between interleukin-18 (IL-18) gene polymorphisms and rheumatoid arthritis (RA) susceptibility. The electronic databases Ovid MEDLINE, Ovid Excerpta Medica Database, and Cochrane Library were searched to identify meta-analyses that included case-control studies reporting IL-18 gene polymorphisms and RA susceptibility. Data were reanalyzed using Review Manager Software 5.1, and Mantel-Haenszel random effects were applied for the five genetic models: allelic, recessive, dominant, homozygote, and heterozygote. The effect size of odds ratios (ORs) and their corresponding 95% confidence interval (CI) were calculated. A total of seven meta-analyses with poor quality were included. The IL-18 polymorphisms -607 A/C, -137 C/G, -920 T/C, and -105 C/A have been reported. With weak evidence, IL-18 -607 A/C polymorphisms were associated with a reduced risk of RA susceptibility using the allele model (OR = 0.76, 95% CI: 0.61 - 0.93, p=0.01), dominant model (OR = 0.67, 95% CI: 0.50 - 0.90, p=0.008), homozygote model (OR = 0.57, 95% CI: 0.35 - 0.91, p=0.02), and heterozygote model (OR = 0.71, 95% CI: 0.54 - 0.93, p=0.01) in the overall population. IL-18 gene polymorphisms and RA susceptibility are affected by ethnicity: With weak evidence, IL-18 -137 C/G polymorphisms were related to reduce RA susceptibility in the Asian population (allele model: OR = 0.59, 95% CI: 0.40 - 0.88, p=0.01; dominant model: OR = 0.57, 95% CI: 0.37 - 0.89, p=0.01; heterozygote model: OR = 0.60, 95% CI: 0.38 - 0.94, p=0.03). IL-18 -607 A/C gene polymorphisms are a protective factor for RA susceptibility in the overall population, and IL-18 -137 C/G gene polymorphisms are a protective factor for RA susceptibility in the Asian population. Further studies are needed to confirm these results owing to the limitations of the included studies.

Genetic insights into endurance athlete status: A meta-analysis of ACVR1B, AGT, FTO, IL-6, and NRF2 gene polymorphisms.

The aim of this meta-analysis was to analyze allele and genotype pattern frequencies of five different gene polymorphisms associated with endurance athlete status. Endurance sports require prolonged physical performance, and it is well known that physiological and genetic characteristics play a prominent role in this performance. In recent years, research on the impact of genetic factors on endurance athlete status has been on the rise, suggesting that various gene polymorphisms may be associated with physical performance. Specifically, the gene polymorphisms, activin receptor type-1B (A9CVR1B) rs2854464, angiotensinogen (AGT) rs699, fat mass and obesity-associated (FTO) rs9939609, interleukin-6 (IL-6) rs1800795, and nuclear factor erythroid 2 (NRF2) rs12594956, are thought to be related to endurance athlete status. Each of these genes plays a part in different biological processes, such as muscle development, energy metabolism, inflammation, and antioxidant defense mechanisms. For example, the NRF2 gene is a critical player in the regulation of cellular stress responses and may contribute to adaptive responses that enhance performance in endurance athletes. This meta-analysis included a total of 20 articles published between 2009 and 2023. The specific gene polymorphisms explored in this study, i.e., ACVR1B rs2854464, AGT rs699, FTO rs9939609, IL-6 rs1800795, and NRF2 rs12594956, were selected due to their reported associations with physical performance and endurance. A comprehensive search was conducted in the Web of Science and PubMed databases using specific keywords, preliminarily identifying 329 articles. Upon analysis of the abstracts, and full texts, 20 articles were deemed eligible for inclusion in this meta-analysis. Articles lacking control and endurance athlete groups or clear allele/genotype data were excluded. The findings indicated no significant differences in allele and genotype frequencies for ACVR1B, AGT, FTO, and IL-6 gene polymorphisms between endurance athletes and control groups. However, the NRF2 rs12594956 gene polymorphism showed a significantly higher frequency of the major allele (A) and the AA genotype in endurance athletes than in controls. In conclusion, the NRF2 rs12594956 polymorphism may be a genetic variant of interest in determining the status of endurance athletes. These findings highlight the potential clinical implications for genetic screening and personalized training programs in sport genetics. More extensive studies with larger cohorts are needed to further confirm these associations.

Interleukin-8 genetic polymorphism and its relation to Helicobacter pylori infection and Helicobacter pylori-associated gastric diseases

Helicobacter pylori (H. pylori) infection has a variety of clinical outcomes, and host genetic factors play an important role in this process. Cytokines are important factors in mediating and controlling the inflammatory process during H. pylori infection. Interleukin-8 (IL-8) plays a critical role in the epithelial cell response to H. pylori infection and the development of H. pylori-related gastric disorders. The IL-8 gene has an A/T base pair polymorphism in the promoter region (-251), which has been linked to an increase in interleukin production by gastric epithelial cells. In this context, the goal of our study was to determine the polymorphism in the IL-8 gene and its relation to H. pylori infection and H. pylori-associated gastric diseases. Gastric biopsy specimens were collected from 44 patients with H. pylori infection and 29 patients without H. pylori infection. The rapid urease test and detection of the glmM gene were used to diagnose H. pylori infection. Polymerase chain reaction-restriction fragment length polymorphism was used to identify the polymorphism in the Il-8 gene (at position-251). The presence of the A/A and T/A genotypes of the IL-8 gene was found to be significantly associated with susceptibility to H. pylori infection (p = 0.012 and p = 0.004, respectively). Also, the IL-8 A allele was significantly associated with H. pylori infection in our study (p = 0.002). We did not find a significant association between IL-8 gene polymorphism and a higher risk of gastritis and peptic ulcer disease. In conclusion, IL-8 gene polymorphism at -251 position was significantly associated with H. pylori infection.

Genetic polymorphism of IL-18 influences susceptibility to lung cancer in population of eastern China.

The association of Interleukin-18 (IL-18) genetic polymorphism with lung cancer risk has yielded inconsistent findings in previous studies. The current research aims to clarify the relationship of IL-18 gene polymorphism with lung cancer susceptibility through experimental investigation and meta-analysis, providing insights for lung cancer prevention and treatment. We conducted a thorough search of major databases from their inception until March 2024. OR and 95%CI were calculated to know the results of meta-analysis. The IL-18 gene polymorphism was detected using the PCR-RFLP method. Significant associations were detected across all genetic models in allele contrast (A vs. C: Odds Ratio [OR] = 1.29, 95% Confidence Interval [CI] = 1.07-1.55, p = 0.006), homozygote comparison (AA vs. CC: OR = 1.87, 95%CI = 1.34-2.62, p < 0.001), recessive genetic model (AA vs. CT/CC: OR = 1.54, 95%CI = 1.08-2.20, p = 0.018), and dominant genetic model (AA/AC vs. CC: OR = 1.41, 95%CI = 1.12-1.78, p = 0.003). Three genotypes (AA, AC, and CC) were identified for the IL-18 -607 C/A polymorphism, with significant associations noted for the AA genotype and A allele (p = 0.018 and 0.005, respectively). This is the first study which investigates this polymorphism with lung cancer in population of eastern China. The IL-18 -607 C/A polymorphism appears to significantly increase the risk of lung cancer in the population of Eastern China. Further research is imperative to validate these findings.

Association Between Interleukin-6 Gene Polymorphism and Severity of Coronary Artery Disease in Patients with Diabetes [Letter

Association Between Interleukin-6 Gene Polymorphism and Severity of Coronary Artery Disease in Patients with Diabetes [Letter

Association Between Interleukin-6 Gene Polymorphism and Severity of Coronary Artery Disease in Patients with Diabetes [Letter

Association Between Interleukin-6 Gene Polymorphism and Severity of Coronary Artery Disease in Patients with Diabetes [Letter

Human visceral leishmaniasis and polymorphisms in interleukin-coding genes: a systematic review.

Visceral leishmaniasis (VL) is a neglected disease that is typical of tropical and subtropical parts of the world and is caused by the trypanosomatid Leishmania donovani complex. This disease is a multifactorial condition that involves parasitic, environmental, and immunogenetic characteristics. Genetic changes in genes encoding cytokines may be associated with changes in their expression and, consequently, with the development of clinical resistance or susceptibility to the disease. This systematic review and meta-analysis aimed to assess whether single nucleotide polymorphisms (SNPs) in interleukin genes influence the clinical consequences of visceral leishmaniasis infection. To this end, we carried out a systematic review and meta-analysis with structured searches in the EMBASE, PubMed, Scopus, SciELO, and Web of Science databases without time restrictions. Two independent reviewers examined the studies, performed data extraction, and assessed quality by assigning scores. If there were any discrepancies, a third reviewer with more experience was consulted. After the screening process, 28 articles were included in the systematic review and 9 in the final analysis of the meta-analysis. Statistical analyses were carried out using various genetic models. The odds ratio (OR) and corresponding 95% confidence intervals (CIs) were calculated to estimate the associations. Overall, the main clinical outcomes were classified as not associated or associated when they presented susceptibility, resistance, risk, or protective factors for the development of the disease. Associations between IFN-γ +874T/A polymorphisms in the dominant model (OR 1.64, 95% CI 1.13-2.38, I2 = 0%, p < 0.01) and heterozygous model (OR 1.72, 95% CI 1.15-2.57, I2 = 0%, p < 0.01) and IL-18 -137G/C in the recessive model (OR 1.33, 95% CI 1.02-1.71, I2 = 9%, p = 0.03) and VL were observed. For the IL-10 gene SNPs, there was no significant association. Our findings suggest that SNPs in the IFN-γ and IL-18 genes may be associated with the risk of developing VL.

Interleukin-6 gene polymorphism (rs1800796) in patient with diabetic nephropathy among Balinese

Background: Diabetic Nephropathy (DN) is the most common complication of diabetes mellitus. Interleukin 6 (IL-6) known as pro-inflammatory cytokine increases extracellular matrix expression and proliferation in DN progression. One single nucleotide polymorphism (SNP) of the Interleukin (IL)-6 gene, rs1800796 play a role in the progression of DN among Asian. Objective: This research seeks to investigate the correlation between IL-6 gene polymorphism (rs1800796) and diabetic nephropathy in individuals diagnosed with type 2 diabetes mellitus (T2DM) among the Balinese population.Methods: This research employed an observational approach through a case-control design involving a total of 60 subjects for each group selected by a simple random sampling method. The occurrence of the rs1800796 polymorphism was identified through polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The genotype and allele distribution acquired in this study were assessed using the chi-square (χ2) test and Hardy-Weinberg equilibrium law.Results: There were no significant differences identified in the occurrence of (DN) based on the genotype or allele distribution of the IL-6 gene rs1800796. Genotype CG-GG had a higher risk of becoming DN with Odd ratio 1.230, but not statistically significant (p=0.577). Allele G with OR 1.198 (p=0.502) was not significant in causing DN. Conclusion: No significant association was identified between IL-6 polymorphism (rs1800796) and diabetic nephropathy in Balinese individuals with type 2 diabetes mellitus. The lack of association could be due to the presence of other haplotypic connections or might require a larger sample size for conclusive results.

Associations among gene polymorphisms, crestal bone loss, and bone mineral density in patients receiving dental implants

ObjectivesInterleukin 1 (IL-1) and interleukin 6 (IL-6) gene polymorphisms have been suggested to be responsible for diminished bone mineral density (BMD) and high crestal bone loss (CBL) in some individuals. However, the effects of systemic BMD on variations in peri-implant CBL are unclear. Hence, this study was aimed at investigating the association of IL-1 and IL-6 gene polymorphisms with systemic BMD and CBL around dental implants. MethodsA total of 190 participants undergoing dental implantation in the mandibular posterior region were selected according to predetermined selection criteria and divided into a normal BMD group (NBD, 93 participants, T-score ≥ −1) and low BMD group (LBD, including both osteoporosis and osteopenia, 97 participants, T-score < −1 standard deviation) according to the BMD of the right femoral neck, measured with dual-energy X-ray absorptiometry. Dental implants were placed through the standard surgical protocol, and CBL was calculated after 6 months with cone beam computed tomography scans before second-stage surgery. Genotyping was performed on all participants for IL-1A-889 A/G, IL-1B-511G/A, IL-1B+3954, and IL-6-572 C/G gene polymorphisms. ResultsThe demographic and clinical characteristics of the participants in both groups were compared with t-test and chi-square test (χ2). The associations of NBD and LBD with the different genotypes and CBL was determined with odds ratios, and p < 0.05 was considered statistically significant. The frequency of IL-1B-511AA and IL-6-572 GG genotypes was significantly higher in LBD than in NBD (p < 0.05). In LBD, the IL-1B-511 AA (AA vs GA + GG; p ≤ 0.001) and IL-6-572 GG (GG vs CC + GC; p = 0.001) genotypes were significantly associated with higher peri-implant CBL. ConclusionsIndividuals with the IL-1B-511 AA or IL-6-572 GG genotype had elevated risk of osteoporosis/osteopenia and were more susceptible to CBL around dental implants.

Monoclonal Antibody Against Mature Interleukin-18 Ameliorates Colitis in Mice and Improves Epithelial Barrier Function.

Antitumor necrosis factor (TNF)-α antibodies have improved the outcome of inflammatory bowel disease (IBD); but half of patients remain unresponsive to treatment. Interleukin-18 (IL-18) gene polymorphism is associated with resistance to anti-TNF-α antibodies, but therapies targeting IL-18 have not been clinically applied. Only the mature protein is biologically active, and we aimed to investigate whether specific inhibition of mature IL-18 using a monoclonal antibody (mAb) against a neoepitope of caspase-cleaved mature IL-18 could be an innovative treatment for IBD. The expression of precursor and mature IL-18 in patients with UC was examined. Colitis was induced in C57/BL6 mice by administering dextran sulfate sodium (DSS), followed by injection with anti-IL-18 neoepitope mAb. Colon tissues were collected and subjected to histological analysis, immunohistochemistry, immunoblotting, and quantitative polymerase chain reaction. Colon epithelial permeability and microbiota composition were analyzed. Mature IL-18 expression was elevated in colon tissues of patients with active ulcerative colitis. Administration of anti-IL-18 neoepitope mAb ameliorated acute and chronic DSS-induced colitis; reduced interferon-γ, TNF-α, and chemokine (CXC motif) ligand-2 production and epithelial cell permeability; promoted goblet cell function; and altered the intestinal microbiome composition. The suppressive effect of anti-IL-18 neoepitope mAb was superior to that of anti-whole IL-18 mAb. Furthermore, combination therapy with anti-TNF-α Ab suppressed acute and chronic colitis additively by suppressing cytokine expressions and reducing cell permeability by upregulating claudin1 and occludin expression. Anti-IL-18 neoepitope mAb ameliorates acute and chronic colitis, suggesting that this mAb will be an innovative therapeutic option for IBD.

Association of the interleukin-10 (IL-10) gene polymorphisms with ovarian cancer risk: a systematic review and meta-analysis

Background. Ovarian cancer is a cancer with high fatality due to its symptomless nature which leads to late diagnosis. Therefore, there is an urgent need to discover genetic markers which are related to predisposition to the disease. With anti-inflammatory cytokines playing a major role in cancer predisposition, the present systematic review and meta-analysis was undertaken to evaluate the association of the interleukin-10 (IL-10) gene polymorphisms with ovarian cancer risk. Material and methods. Online databases were searched for articles dating from June 2023 until inception for studies assessing the frequencies of IL-10 polymorphisms in ovarian cancer patients and controls. The odds ratios of the genotypes alongside with their respective 95% confidence intervals were calculated under three different genetic models. Results. A total of 5 records studying the IL-10-819 C&gt;T and IL-10-1082 G&gt;A polymorphisms were included in the quantitative analysis. The meta-analysis suggested that the IL-10-819 C&gt;T polymorphism was significantly associated the risk of ovarian cancer under a dominant (CT + TT vs CC) inheritance model (OR = 2.67; 95% CI = [1.17,6.12]; p = 0.02). Conclusions. The meta-analysis suggested that the T allele of the IL-10-819 C&gt;T is associated with increased risk of ovarian cancer, but there is no statistically significant association between the IL-10-1082 G&gt;A polymorphism and ovarian cancer. Future studies are required to further verify these results.

Association of Interleukin-10 Gene Polymorphism with Susceptibility and Severity of Axial Spondyloarthritis

Background: This study aimed to determine the association of Interleukin-10 (IL-10) gene polymorphisms with the susceptibility and severity of axial spondyloarthritis (axSpA) that may guide to have an idea about the genetic basis of the disease and it’s association with severity. Objective: Aim of the study was to demonstrate the IL-10 gene polymorphisms to determine their association with susceptibility and severity of axSpA. Methods: According to Assessment of Spondyloarthritis International Society (ASAS) classification criteria total 38 patients with axSpA (clinically diagnosed by an expert Rheumatologist, attending in outpatient department (OPD) of Rheumatology, Bangabandhu Sheikh Mujib Medical University, BSMMU) and 38 healthy controls (resident doctors, laboratory staffs of BSMMU and general people) after fulfilling the inclusion criteria were enrolled in this study. Blood samples were collected after taking informed written consent and data were collected in a predesigned data collection sheet. The IL-10 gene polymorphisms IL-10 (819T/C), IL-10 (1082A/G) and IL-10 (592C/A) were detected by Polymerase chain reaction- Restriction fragment length polymorphism (PCR- RFLP) method at Department of Microbiology and Immunology, BSMMU, Dhaka. Results: According to BASDAI score, 14 patients were in inactive disease group and 24 patients were in active disease group. The homozygous CC genotype and C allele of IL-10 (-819T/C) were found significantly higher in patients than control group (p=0.022 and p=0.045 respectively). The heterozygous GA genotype of IL-10 (-1082A/G) gene has significant association (p=0.001) with axSpA. It indicates that the homozygous CC genotype and C allele of IL-10 (819T/C) and heterozygous GA genotype of IL-10 (1082A/G) have an association with the susceptibility of axSpA. Conclusion: CC genotype and C allele of IL-10 (-819T/C) and GA genotype of IL-10 (1082A/G) are associated with axSpA susceptibility. But no association of these genotypes were found with disease severity. Bangladesh Med Res Counc Bull 2023; 49: 171-176

Interleukins-6 −174G/C (rs1800795) and −572C/G (rs1800796) polymorphisms and prostate cancer risk

Prostate cancer (PCa) is an aggressive cancer influenced by a complex interplay of genetic and environmental factors. Amongst these risk factors, the impact of Interleukin6 (IL6) gene polymorphisms in PCa risk has received a lot of attention. IL-6 is a cytokine that has been implicated in the pathogenesis of several malignancies, including PCa. Two IL-6 gene polymorphisms, − 174 G/C (rs1800795) and − 572 C/G (rs1800796), have received intellectual attention due to their potential role as modulators of prostate cancer risk. The main objective of this research was to comprehensively explore the potential associations between IL-6 rs1800795 and rs1800796 polymorphisms, and their impact on the occurrence of PCa. A case-control study was carried out with a well-defined cohort comprising 110 PCa cases and 110 controls (total n = 220). The genotyping of rs1800795 and rs1800796 was carefully performed using the highly sensitive and accurate Polymerase Chain Reaction-High Resolution Melting Curve (PCR-HRM) technique. The assessment of genetic associations was evaluated using various R packages, such as Haplo-Stats, SNP stat, pheatmap, and LD heatmap. The present study applied odds ratio (OR) analysis to reveal significant evidence of strong associations between the genotypes of rs1800795 and rs1800796 and the susceptibility to PCa. The findings of this study underscore the noteworthy impact of genetic variations in the IL-6 gene on the development of prostate cancer. Specifically, the C/G and G/G genotypes of rs1800795 demonstrated increased PCa risk, with odds ratios (OR) of 1.650 (95% CI = 1.068–2.549, p = 0.032) and 2.475 (95% CI = 1.215–5.043, p < 0.001), respectively. Similarly, the G/C genotype of rs1800796 exhibited an OR of 2.374 (95% CI = 1.363–4.130, p = 0.012) for elevated prostate cancer risk, while the C/C genotype had an OR of 1.81 (95% CI = 1.02–3.22, p = 0.7). Furthermore, our haplotype analysis have revealed an association between haplotype 4 (C-G) and increased risk of PCa (OR = 1.69, 95% CI = 1.05–2.73, p = 0.032). In conclusion, this case-control analysis presents compelling evidence for a significant association between IL-6 variants (rs1800795 and rs1800796) and increased susceptibility to prostate cancer.

Association Between Interleukin-6 Gene Polymorphism and Severity of Coronary Artery Disease in Patients with Diabetes.

Previous studies have identified diabetes as a risk factor for coronary heart disease. This study determined the correlation between the IL-6 gene -572 G/C polymorphism and the incidence and severity of coronary heart disease in patients with diabetes. One hundred four patients with diabetes who were admitted to our hospital from January 2019 to December 2020 were retrospectively enrolled in the current study. These patients were divided into a diabetes only group (group A, 27 patients) and a diabetes complicated by coronary heart disease group (group B, 77 patients). Seventy patients in the latter group were further divided into low, medium, and high Syntax score groups based on coronary angiography results. A correlation analysis between IL-6, blood lipids, and the IL-6 -572 G/C gene levels was performed. The serum IL-6 level in patients with the IL-6-572G/C-GG genotype was higher than patients with the GC and CC genotypes. In patients with diabetes, the presence of the IL-6-572G/C-GG and GC genotypes was associated with a significantly increased risk of developing coronary heart disease. Patients with the IL-6-572G/C-GG genotype and diabetes were shown to have more severe coronary artery lesions compared to patients with the CC genotype. Moreover, the G allele of the IL-6-572G/C gene was linked to a higher risk of coronary heart disease and more severe coronary artery lesions in patients with diabetes compared to the C allele. The IL-6-572G/C gene polymorphism is associated with the incidence and severity of coronary heart disease in patients with diabetes.

Interleukin-4 (C590T) Gene Polymorphism in Association with Asthma Severity.

A significant link between T allele of the IL-4 (C590T) gene and developing asthma in some populations was reported. However, no study discussed the link between IL-4 (C590T) gene polymorphism and asthma severity groups (mild and severe). This study investigated the link between IL-4 gene variation and asthma severity. The study included 215 asthmatic patients, of which 102 had mild asthma, and 126 participants were healthy controls. A previously published polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method was used to identify various IL-4 (C590T) gene polymorphism genotypes. The T allele frequency was higher in mild asthma (p=0.002) but not in severe asthma (p=0.12) compared to controls. In mild asthma, the CT genotype and (CT+TT versus CC) increased the likelihood of asthma threefold (p<0.001, 0.001). However, no significant association with severe asthma was found in either genetic model. Stratification analysis showed that the C allele and CC genotype increased the risk of severe asthma (p=0.01). The recessive genetic model indicated a decrease in the risk of severe asthma (OR=0.5, p=0.01) in the non-adjusted regression analysis. Adjusting for age, sex, and other risk factors revealed that the IL-4 gene polymorphism did not influence the risk of severe asthma (OR=0.92, p=0.80); however, being an elderly female with a history of childhood-onset disease and associated nasal polyp (NP) increased the likelihood of severe asthma, OR=1.08, 2.01, 2.36, 8.42; p<0.001, 0.05, 0.05, <0.001, respectively. The T allele and CT genotype in the co-dominant genetic model and the (CT+TT) genotype in the recessive model were found to have a higher likelihood of developing mild asthma but not severe asthma; severe asthma was found to be higher in elderly females with a history of childhood-onset disease and associated nasal polyps.

The role of IL-13 gene polymorphism in the exacerbation of Asthma severity

Asthma is a chronic airway inflammatory disorder characterized by persistent inflammation, obstruction, and hyperresponsiveness. The role of cytokines, particularly Interleukin-13 (IL-13), in the pathogenesis of asthma has been extensively studied. IL-13 is involved in Th2 inflammation and has been identified as a possible therapeutic target in asthma treatment. This review focuses on the role of IL-13 gene polymorphism in exacerbating asthma severity. IL-13 is responsible for various key pathological features of asthma, including airway hyper- responsiveness, mucus production, and induction of allergic responses. The release of IL-13 is triggered by exposure to allergens, which activate dendritic cells and promote the differentiation of Th2 cells. IL-13 interacts with its receptors, IL-13Rá1 and IL-13Rá2, and initiates signaling pathways involving JAK1, JAK3, and STAT6. Biomarkers such as total serum IgE, exhaled nitric oxide (FeNO), airway epithelial proteins, blood eosinophil counts, and sputum eosinophil counts have been used to assess IL-13 activity and predict treatment response. Polymorphisms in the IL-13 gene and its receptors have been associated with asthma susceptibility, severity, and response to therapy. Understanding the role of IL-13 gene and polymorphism in asthma can provide insights into disease mechanisms and contribute to personalized treatment approaches. Further studies are needed to elucidate the association airway between IL-13 polymorphisms, asthma severity, and response to inhaled corticosteroids (ICS).&#x0D;

Hubungan Polimorfisme Gen Interleukin 10 - 819 C/T Pada Kejadian Preeklampsia Ibu Hamil di Puskesmas Dalu X B Tanjung Morawa Deli Serdang

Preeclampsia is one of the disorders during pregnancy, characterized by increased blood pressure and proteinuria, causing an increase in morbidity and mortality in the mother and fetus. Interleukin 10 (IL10) is called a T helper type 2 (Th2) cytokine which is important because it acts as an anti-inflammatory which functions for the maintenance and development of pregnancy and forms immunity to inhibit the secretion of T helper 1 (Th1) cytokines such as IL 6, TNF alpha and INF Gamma. Genotypic variation can provide information about individual differences in the secretion of IL-10 and the tendency to the incidence of preeclampsia. The IL 10 - 819 C/T gene polymorphism is located on chromosome 1q32.2 distal to the promoter area and is a transcription factor of the IL 10 gene. The aim of this study was to determine the relationship between 10-819 C/T Interleukin Gene Polymorphisms in the incidence of preeclampsia in pregnant women. The method used to determine the IL 10 819 C/T polymorphism with RFLP PCR. Results. The distribution of IL 10-819 C/T genotypes in the control group had 5 people (23.73%) of TT genetic variation, 15 people with CT (65.21%) and 3 people with CC genetic variation (13.04%). ). In the Preeclampsia group, there were 7 people (30.43%) with genetic variation of TT and there were 10 people (43.47%) with genetic variation of CT as many as 6 people (26.08%) with CC variation. There was no correlation between interleukin gene polymorphism 10-891 C/T with the incidence of preeclampsia in pregnant women at Dalu X B Health Center Tanjung Morawa, Deli Serdang

Effect of interleukin-2 (IL-2) polymorphisms on multiple myeloma: IL-2RA rs2104286, IL-2 rs2069762 and rs2069763 polymorphisms

Interleukin-2 (IL-2) is a cytokine secreted from T helper type 1 cells and released after induction of T helper cells with major histocompatibility complexes or antigens presented by antigen presenting cells. IL-2 activity and gene polymorphisms have been studied in both solid and hematological malignancies. In the present study, it was aimed to examine the effects of IL-2RA rs2104286, IL-2 rs2069762 and rs2069763 polymorphisms on multiple myeloma (MM) susceptibility, progression-free survival (PFS) and overall survival (OS). A total of 300 patients diagnosed with MM in our clinic between January 2010 and January 2021, and 170 healthy individuals were included. In addition to the demographic data of the patients, MM subtypes, initial stages, prognostic index scores, laboratory results, treatment preferences, and survival data were recorded. The genotypes of the IL-2RA rs2104286, IL-2 rs2069762 and rs2069763 polymorphisms were statistically compared between patients and healthy controls to reveal their effects on MM susceptibility and survival. In the statistical analysis performed to examine the effect of IL-2RA rs2104286, IL-2 rs2069762 and rs2069763 polymorphisms on disease susceptibility, no significant difference was found between the patient and healthy control groups. Patients with the TG genotype of IL-2 rs2069762 had a significantly shorter median PFS and OS compared to others. Patients with the GG genotype of IL-2 rs2069763 had a significantly shorter median PFS compared to others. Having the TG genotype of IL-2 rs2069762 has been shown to be protective for short PFS and OS. Our study results will be guiding in terms of IL-2 based therapies, the future for MM and MM epigenetics.

Study the Association between Interleukin-4 Polymorphism and Specific Chlamydia Pneumoniae Immunoglobulin E in Asthmatic Children

Background: Asthma is a chronic disorder caused by complex interactions between genetic and environmental influences. Objective: Investigate the possible correlation between interleukin-4 (IL-4) gene polymorphisms and development of specific Chlamydia pneumoniae immunoglobulin (Ig) E levels. Materials and Methods: A total of 87 children, including 57 males and 30 females with asthma with ages between 1 and 16 years, attended the Respiratory Clinic at Karbala Pediatric Hospital, with a nonasthmatic children group which have the same age and gender. Restriction fragment length polymerase chain reaction was performed to determine IL-4 C-589T genetic polymorphisms. Total IgE level, C. pneumoniae IgG, and C. pneumoniae IgE antibodies were measured using the commercial quantitative enzyme-linked immunosorbent assay kits. Results: C. pneumoniae IgG and IgE antibodies were significantly increased in patients as compared with controls (P &lt; 0.001 and P = 0.024, respectively). The CT genotype of IL-4 C-589T polymorphism was associated with asthmatic children (P &lt; 0.01). A high C. pneumoniae IgE levels were found to be associated with CC genotypes (P = 0.01). On the other hand, there were no significant differences in serum C. pneumoniae IgG levels depending on different IL-4 C589T genotypes (P = 0.662). Conclusion: The development of C. pneumoniae IgE antibody in asthmatic children did not depend on IL-4 polymorphism.