IL-10 Polymorphisms Research Articles

Pro-inflammatory and anti-inflamatory cytokine genes polymorphisms and susceptibility to Japanese encephalitis disease in the North Indian population.

Japanese encephalitis virus (JEV) is the major cause of viral encephalitis in many regions of Asia. Cytokines, including pro-inflammatory and anti-inflammatory are key regulators playing a detrimental role in the host response to JE infection, pathogenesis and disease outcome. Evidently, the host's cytokine response is genetically determined, representing the complexity of interindividual differences regarding immune response to viral infection. The current study assesses the association of single nucleotide polymorphisms of classical interleukin IL-1β and IL-10 with JEV susceptibility and disease severity in north Indian population. We performed a case-control study using 85 JE patients and 85 healthy controls. Polymorphisms in the IL-1β (-511 C/T) and IL-10 (-1082 A/G) genes were genotyped using PCR-RFLP. All continuous variables were expressed as mean±standard deviation, and categorical variables were expressed in percentage. The mRNA level of IL-1β and IL-10 were found significantly increased in JE patients. In severe JE patients, IL-1β mRNA level was significantly higher with heterozygous (C/T) and homozygous (C/C) genotype compared to wild (T/T) genotype and mRNA level of IL-10 was higher in heterozygous genotype (A/G) compared to wild genotype (A/A). The C/T and C/C genotypes of IL-1β were significantly associated with higher risk of JE infection (p<0.05, OR=7.25 and 4.40) whereas, the A/G genotype of IL-10 was associated with a reduced risk of JEV infection (p<0.05, OR=0.30). The C allele of IL-1β was associated with fever and neck stiffness (p<0.05) and CT genotype was associated with disease severity and worse outcomes in JE patients. Along with this, IL-10 polymorphism was found associated with fever, and AG genotype was found to be associated with worse disease outcomes such as neurological sequelae (p<0.05). Mutant allele and genotype at IL-1β (-511 C/T) and IL-10 (-1082 A/G) gene polymorphism show increased expression of IL-1β and IL-10 in JE patients which contribute to disease severity as well as adverse outcomes of disease. Overall this is the first report from northern India, which shows the association of IL-1β and IL-10 polymorphisms with JEV infection.

IL-10 and TGF-β1 gene polymorphisms in Greek patients with recurrent aphthous stomatitis.

Background Recurrent aphthous stomatitis (RAS) is one of the most frequent inflammatory disorders of the oral mucosa. Cytokines, which play an important role in RAS pathogenesis, participate directly or indirectly in normal, immunological and inflammatory processes and are secreted from cells belonging to innate and adaptive immunity as a consequence of microbial and antigenic stimuli. Gene polymorphisms in specific cytokines may predispose to RAS development. The aim of this study was the investigation and association of IL-10 and TGF-β1 gene polymorphisms with RAS.Material and Methods Study’s cohort consisted of 60 Greek patients diagnosed with RAS, including 40 patients with minor, 10 patients with major and 10 with herpetiform aphthous ulcers. Forty age- and sex-matched control subjects were included in this study. DNA was extracted from whole blood samples of all patients and sequence-specific primers (SSP)-based polymerase chain reaction (PCR) was used for genotyping. Gene polymorphisms for cytokines IL-10 at loci -592 and -819 and for TGF-β1 at codon 10 were detected.Results Significant differences between patients with minor RAS and healthy controls were recorded for IL-10 genotypes distribution at position -592 (p=0.042) and -819 (p=0.045) with predominance of C/A and C/T genotypes in RAS patients, respectively. Also, in patients with minor and herpetiform aphthous ulcerations, heterozygous TGF-β1 genotype C/T at codon 10 was associated with increased risk of RAS (p=0.044 and p=0.020, respectively).Conclusions These data provide evidence that genetic predisposition for RAS and possibly its specific clinical variants is related with the presence of gene polymorphisms for specific cytokines, including IL-10 and TGF-β1, which, in turn, may vary according to geographic origin and genetic background. Key words:Recurrent aphthous stomatitis, aphthae, IL-10, TGF-β, gene polymorphisms, oral mucosa.

The role of cytokine gene single nucleotide polymorphism in the development of recurrent acute otitis media

The study aimed at examining the role of single nucleotide polymorphism (SNP) of cytokine genes in the development of recurrent acute otitis media (AOM) among children. Single nucleotide polymorphism of IFN-, IL-6, IL-10, TNF-α, and TGF-β1, were analyzed by the polymerase chain reaction with sequence-specific primers (PCR-SSP) in 82 children with recurrent AOM and compared with a similar control group. There was a significant higher incidence of IL-10 polymorphisms (loci -592, -819 and -1082) in children with recurrent AOM (P=0.0137, 0.0137 and 0.0072, respectively). However, there was no significant difference in the distribution of other cytokine genotypes between the two study groups. Among the 5 studied cytokine genes, only IL-10 loci showed significant correlation to the development of recurrent AOM.

Genetic polymorphism of cytokines IL-1β, IL-4 and TNF-α as a factor modifying the impact of childhood adversity on schizophrenia symptoms

Based on the hypothesis that activation of the immune system is one of the mechanisms of influence of early environmental factors on the onset and course of schizophrenia, we investigated the effects of the interaction of childhood adversity and IL-1β rs16944, IL-4 rs2243250 and TNF-α rs1800629 polymorphisms on schizophrenia symptomatology. The sample consisted of 546 patients with schizophrenia spectrum disorders. The presence of childhood adversity was determined based on the analysis of medical records and a questionnaire completed by the patient. We used the 5-factor model of the Positive and Negative Syndrome Scale (PANSS) with the nested two-factor negative syndrome model. After adjusting for multiple comparisons, a significant effect of the interaction of childhood adversity and TNF-α on the cognitive/disorganization factor was found, with a difference between genotypes in the group without childhood adversity (pFDR <0.018; η2p=0.03). A significant effect of the interaction of childhood adversity and genotype on the cognitive disorganization syndrome was established (F=5.87; p=0.003; η2p=0.03). Stereotyped thinking and avolition on PANSS had the highest correlations with cognitive disorganization factor (ro=0.84 and ro=0.82, respectively) and the highest significance of differences depending on the interaction of genotype and childhood adversity (Kruskal-Wallis test, H=12.28, p=0.006 and H=12.79, p=0.005, respectively). Childhood adversity modifies the relationship between the pathogenesis of schizophrenia and the TNF-α promoter polymorphism rs1800629, which is also an enhancer of another 60 genes located in the major histocompatibility complex.

The role of some genetic polymorphisms of IL-10 in the development of varicella in military personnel

The role of some genetic polymorphisms of IL-10 in the development of varicella in military personnel

Associations of IL-6 polymorphisms with Behçet’s Disease in Denizli, province of Turkey

Behçet's Disease is a chronic, multisystemic disease and the etiopathogenesis of the disease develop as a result of the interaction of environmental and genetic factors. IL-6 is a proinflammatory cytokine with functions on immune response regulation and chronic inflammation demonstrated by increased serum levels and gene expression studies in Behçet’s disease. We genotyped IL-6; rs1800797, rs1800796 and rs1800795 polymorphisms in 78 patients with Behçet’s disease and 130 healthy controls using PCR-RFLP based approach. No statistically significant difference in allele or genotype frequencies of IL-6, rs1800797 and rs1800796 was found in between groups. We determined that in the BD patients with genital ulcers, arthritis and without vascular involvement was found to have significantly different IL-6, SNP frequencies compared with healthy controls. In addition, the IL-6 rs1800795 GC genotype and C allele may contribute to the development of the disease in female BD. The haplotype distributions of all loci of IL-6 were examined and GGG was found as the highest frequency haplotype in both groups. In conclusion, the results of our study showed that IL-6 rs1800795 may associate with the susceptibility to the BD. Studies should be conducted with more SNPs in large and different populations need to evaluate the contribution of responsible alleles for the disease and its clinical features.

Single nucleotide polymorphism in Interleukin 1 alpha gene might be involved in the Oral Herpes recurrent episodes in Brazilian Para-Athletes

The main goal of this study was to investigate if there is an association between Oral Herpes (OH) recurrent episodes and Single Nucleotide Polymorphisms (SNPs) in IL1A, IL10, and IL1RN genes in a group of Brazilian Para-athletes. This transversal study was prepared according to the STrengthening the REporting of Genetic Association Studies (STREGA) guidelines. Oral examination and DNA collection for genotyping were performed in a non-probabilistic convenience sampling composed of Brazilian para-athletes who participated in a Brazilian selective competition. Data referring to the general characterization of sample were collected through a self-reported questionnaire. Candidate genes were chosen with the UCSC Genome Browser and SNPs in IL1A gene (rs17561, rs1304037), IL10 gene (rs1800871), and IL1RN gene (rs9005) were selected and investigated in allelic, genotypic, dominant, and recessive models. Hardy-Weinberg equilibrium was evaluated in each SNP. The sample was composed of 273 para-athletes (63 (23.4%) practice swimming, 61 (22.3%) powerlifting and 145 (63.7%) athletics). OH recurrent episodes was related by 47 (17.2%) para-athletes and the presence of T allele in the rs1304037 increased chance of OH. These findings suggest that rs1304037 in IL1A gene is associated with OH recurrent episodes in para-athletes.

Genetic variation and up-regulation of IL-12 enhance susceptibility to recurrent vulvovaginal candidiasis

Objective(s)Approximately up to 9% of women may experience more than three episodes per year of vulvovaginal candidiasis (VVC) that is named as recurrent vulvovaginal candidiasis (RVVC). Genetic factors play an important role in the susceptibility to RVVC. This study was aimed to find the effect of genetic variants of interleukin (IL)-12 genes as well as mRNA expression level for on susceptibility to RVVC caused by Candida albicans. MethodsIn this case-control study, 95 patients with RVVC and 101 healthy controls were enrolled. The expression level and prevalence of polymorphisms in IL-12 was assayed using real-time PCR and ARMS-PCR, respectively. Single nucleotide polymorphisms (SNPs) in IL-12 (rs568408) are associated with the susceptibility to RVVC. ResultsAnalysis of IL-12A gene alleles at rs568408 position showed that 38.94% and 61.06% of the patients had allele A and G, respectively. However, in the healthy control 43.57% and 56.43% had alleles A and G, respectively. This difference in frequency of A and G alleles between the control and patients group was statistically significant. In the present study the highest ratio of IL-12A (rs568408) genotypes for patients with RVVC was belonged to AG (63.15%), followed by GG 29.47%, and AA (7.38%). While, the highest ratio of IL-12A (rs568408) genotypes for the control individuals was belonged to AG (73.26%) followed by AA (19.80%), and GG (6.94%) that was significantly different with the patients. In the patients with RVVC, the mRNA level of IL-12 was significantly up-regulated compared to the control group. ConclusionThe results of this case-control study suggest that the IL-12 rs568408 polymorphism might play a role in the recurrent Candida infections. Genetic variation in IL-12 may significantly enhance susceptibility to RVVC by up-regulation of IL-12 expression. The genotype frequency and A/G alleles at position IL-12 rs568408 in patients with RVVC caused by C. albicans and healthy individuals were significantly different.

Assessment of the role of IL6 and IL10 gene polymorphisms as a risk factor for the development of restenosis in patients after implantation of drug-eluting stents

Relevance. Currently, the number of percutaneous coronary interventions continues to increase, which leads to an increase in the absolute number of restenosis cases, which is the main complication of the long-term postoperative period. The search for risk factors responsible for restenosis and artery re-narrowing mechanisms in order to prevent this complication is an important goal in interventional cardiology. Risk factors for the restenosis development include clinical, angiographic and genetic factors. An active search for biomolecular markers associated with the coronary artery restenosis is currently underway. Objective: to study the role of polymorphic variants C-174G of the IL6 gene and C-819T of the IL10 gene as a risk factor for the development of restenosis in patients after stent implantation. Materials and Methods : The study included 113 patients with stable coronary artery disease, who had previously undergone balloon angioplasty and implantation of drug-eluting stents, and 62 patients with intact arteries that were included to the control group. Statistical data processing was carried out using the R-language program and the SPSS Statistics 20 software package. Results: GG genotype for IL6 gene was associated with the development of coronary artery disease. In the subgroup of patients over 65 years of age and instent restenosis, the GG genotype was significantly less frequent. The homozygous CC genotype for IL10 gene was associated with rapid angiographic in-stent restenosis progression.

Association of IL-9, IL-10, and IL-17 Cytokines With Hepatic Fibrosis in Human Schistosoma mansoni Infection.

This is a case series study to evaluate immunological markers associated with schistosomiasis advanced fibrosis, including 69 patients from an endemic area from the State of Sergipe and from the Hepatology Service of the University Hospital in Sergipe, Brazil. Hepatic fibrosis was classified based on Niamey protocol for ultrasonography (US). Immune response to Schistosoma mansoni antigens was evaluated by stimulating peripheral blood mononuclear cells (PBMCs) from these patients with either adult worm (SWAP—10 μg/ml) or egg (SEA—10 μg/ml) antigens or purified protein derivative of turberculin (PPD—10 μg/ml) or phytohemagglutinin (PHA—1 μg/ml) for 72 h. The levels of IFN-γ, TNF-α, IL-5, IL-10, and IL-17 were measured in these supernatants by ELISA and IL-9 by Luminex. Single nucleotide polymorphisms in IL-17, IL10, and CD209 genes were genotyped using TaqMan probe by qPCR. Higher levels of IL-9, IL-10, and IL-17 were found in PBMC supernatants of patients with advanced hepatic fibrosis. Direct correlations were detected between IL-9 and IL-17 levels with US spleen sizes, portal vein diameters, and periportal thickening. The CD209 rs2287886 AG polymorphism patients produce higher IL-17 levels. Together, these data suggest a role of these cytokines in the immunopathogenesis of advanced fibrosis in human schistosomiasis.

Periodontitis association with IL-8 gene polymorphisms.

IL-8 and its polymorphisms are involved in multiple acute and chronic inflammatory processes including pathological changes to surrounding structures of the teeth called periodontal diseases or periodontitis. The aim of this manuscript was to systematically review studies from 2006 to 2021 on IL-8 polymorphisms and their association with periodontitis. Literature analysis was done following the PRISMA protocol guidance using articles not older than 15 years (2006-2021). The search was carried out using PubMed (MEDLINE), ScienceDirect and Wiley Online Library databases. For the focus question, the PICO (population (P), intervention (I), control (C), and outcome (O)) study design protocol was used, and the following question was formulated: are IL-8 gene polymorphisms associated with periodontitis? A total of 2422 articles were found at the beginning of the search. After applying the inclusion and exclusion criteria, screening, and full-text article exclusion with reasons, 31 studies were included in the analysis. In conclusion, IL-8 and its gene polymorphisms are associated with an increased risk of periodontal diseases.

Genetic association study reveals impact of interleukin 10 polymorphisms on cognitive functions in schizophrenia

AimCognitive deficits are the core factors impacting quality of life among patients diagnosed with schizophrenia. Effective method of treatment for this domain of symptoms remains lacking. Recent evidence suggests the link between impaired cognition and aberrant inflammatory response. Severity of symptoms might be linked to individual genetic predispositions and single-nucleotide polymorphisms (SNPs) in genes encoding interleukins and their receptors. Current genetic association studies include anti-inflammatory interleukins, such as IL10. Functional polymorphisms of IL10 (rs1800871, rs18008729) have been indicated to affect information processing in schizophrenia. Materials and methodsIn this study, we analyzed the potential impact of 27 functional SNPs in 8 cytokine genes on cognitive parameters measured by Wisconsin card-sorting test (WCST) in schizophrenia group (n = 150) and healthy controls (n = 152). ResultsWe found significant associations of two functional polymorphisms of IL10 (rs1800871, rs1800872) and WCST results. Allele A carriers in rs1800871 performed significantly better in Percent of Conceptual Level Responses (CLR%). Allele A carriers in rs1800871 and allele T carriers in rs1800872 obtained better results in Completed Categories (CC). The impact of illness duration was observed, with better performance of recent-onset patients. ConclusionsResults of this study indicate that genetic variants of inflammatory response are associated with cognitive deficits in schizophrenia. The role of cytokines in schizophrenia need to be investigated in the aspect of pro-/anti-inflammatory imbalance. Altered inflammatory response promote chronic mild inflammation in the brain and aberrant synaptic plasticity.

Current status and relevance of single nucleotide polymorphisms in IL-6-/IL-12-type cytokine receptors.

Cytokines control immune related events and are critically involved in a plethora of patho-physiological processes including autoimmunity and cancer development. In rare cases, single nucleotide polymorphisms (SNPs) or single nucleotide variations (SNVs) in cytokine receptors eventually cause detrimental ligand-independent, constitutive activation of signal transduction. Most SNPs have, however, no or only marginal influences on gene expression, protein stability, localization and function and thereby only slightly affecting pathogenesis probability. The SNP database (dbSNP) is an archive for a broad collection of polymorphisms in which SNPs are categorized and marked with a locus accession number "reference SNP" (rs). Here, we engineered an algorithm to directly align dbSNP information to DNA and protein sequence information to clearly illustrate a genetic SNP landscape exemplified for all tall cytokine receptors of the IL-6/IL-12 family, including IL-23R, IL-12Rβ1, IL-12Rβ2, gp130, LIFR, OSMR and WSX-1. This information was complemented by a comprehensive literature summary and structural insights of relevant disease-causing SNPs in cytokine/cytokine receptor interfaces. In summary, we present a general strategy with potential to apply to other cytokine receptor networks.

IL-6 and IL-10 gene polymorphisms and cirrhosis of liver risk from a comprehensive analysis

BackgroundDifferent inflammatory and immune cytokines play a key role in the development of cirrhosis of liver (CL). To investigate the association between interleukin-6,10 (IL-6,10) genes polymorphisms and CL risk through comparison of the allele and genotype distribution frequencies by meta-analysis.MethodsA literature search covered with the PubMed, Embase, Cochrane Library, Web of Science, Google Scholar, SinoMed (CNKI and Wanfang) through 20th April, 2021. Odds ratios (OR) and 95% confidence intervals (CI) were used to assess the strength of associations.ResultsAfter a comprehensive search, three common polymorphisms (rs1800872, rs1800871, rs1800896) in IL-10 gene were selected, and three common polymorphisms (rs1800795, rs1800796, rs1800797) in IL-6 gene were also identified. The important finding was that IL-10 rs1800872 was a risk factor for CL development. For example, there has a significantly increased relationship between rs1800872 polymorphism and CL both in the whole group (OR: 1.30, 95%CI: 1.01–1.67 in heterozygote model), Asian population (OR: 1.40, 95%CI: 1.03–1.88 in heterozygote model) and hospital-based source of control (OR: 1.40, 95%CI: 1.01–1.96 in dominant model). In addition, significant association was found between rs1800896 and primary biliary cirrhosis subtype disease (OR: 1.30, 95%CI: 1.01–1.68 in allelic contrast model). No association was observed in all three polymorphisms in IL-6 gene.ConclusionOur present study suggests that the IL-10 rs1800872 and rs1800896 polymorphisms is potentially associated with the risk of CL susceptibility.

TNFA and IL10 Polymorphisms and IL-6 and IL-10 Levels Influence Disease Severity in Influenza A(H1N1)pdm09 Virus Infected Patients

Cytokines are key modulators of immune response, and dysregulated production of proinflammatory and anti-inflammatory cytokines contributes to the pathogenesis of influenza A(H1N1)pdm09 virus infection. Cytokine production is impacted by single nucleotide polymorphisms (SNPs) in the genes coding for them. In the present study, SNPs in the IL6, TNFA, IFNG, IL17A, IL10, and TGFB were investigated for their association with disease severity and fatality in influenza A(H1N1)pdm09-affected patients with mild disease (n = 293) and severe disease (n = 86). Among those with severe disease, 41 patients had fatal outcomes. In a subset of the patients, levels of IL-2, IL-4, IL-6, IL-10, TNF, IFN-γ, and IL-17 were assayed in the plasma for their association with severe disease. The frequency of TNFA rs1800629 G/A allele was significantly higher in severe cases and survived severe cases group compared to that of those with mild infection (OR with 95% for mild vs. severe cases 2.95 (1.52–5.73); mild vs. survived severe cases 4.02 (1.84–8.82)). IL10 rs1800896-rs1800872 G-C haplotype was significantly lower (OR with 95% 0.34 (0.12–0.95)), while IL10 rs1800896-rs1800872 G-A haplotype was significantly higher (OR with 95% 12.11 (2.23–76.96)) in fatal cases group compared to that of the mild group. IL-6 and IL-10 levels were significantly higher in fatal cases compared to that of survived severe cases. IL-6 levels had greater discriminatory power than IL-10 to predict progression to fatal outcome in influenza A(H1N1)pdm09 virus-infected patients. To conclude, the present study reports the association of TNFA and IL10 SNPs with severe disease in Influenza A(H1N1)pdm09 virus-infected subjects. Furthermore, IL-6 levels can be a potential biomarker for predicting fatal outcomes in Influenza A(H1N1)pdm09 virus infected subjects.

The association of rs187238, rs19465518 and rs1946519 IL-8 polymorphisms with acute kidney injury in preterm infants.

BackgroundInterleukin 18 (IL-18) promoter polymorphisms (−656G > T, −607C > A, and −137G > C) affect serum IL- 18 (sIL-18) levels and are associated with renal injury.PurposeThis study aimed to determine the diagnostic utility of sIL-18 and urine IL-18 (uIL-18) as biomarkers for acute kidney injury (AKI) and analyse the association of IL-18 polymorphisms to AKI in preterm infants.MethodsBlood and urine samples were collected from 56 preterm infants with AKI and 56 without AKI to measure serum creatinine (SCr), sIL-18, and uIL-18. Genotyping of polymorphisms was performed and analysed, with AUC-ROCs analysis used to evaluate the diagnostic utility of s-/uIL-18 levels.ResultsThe median sIL-18 and uIL-18 levels were significantly higher than those without AKI. For a cutoff of >132 pg/mL, the sIL-18 expression had sensitivity and specificity of 80.36% and 60.71%, respectively, while for uIL-18, a cutoff of >900.7 pg/mL had sensitivity and specificity of 51.79% and 78.57%, respectively. The odds ratio of sIL-18 and uIL-18 to predict AKI in preterm infants was 5.89 (95%CI:2.31–15.02) and 4.15 (95%CI:1.58–10.89), respectively. The polymorphisms −137G > C and −656G > T were significantly associated with sIL-18 expression.ConclusionSerum and urine IL-18 levels are risk factors for and a moderate predictor of AKI in preterm infants.

M12. Network Meta-Analysis about Cytokine Gene Functional Polymorphisms Towards the Susceptibility and Severity of Acute Rheumatic Fever and Rheumatic Heart Disease among Asian and Non-Asian People

Abstract Background Great diversity among public hereditary variants may play a role in the susceptibility and severity of acute rheumatic fever (ARF)/rheumatic heart disease (RHD). Cytokine gene polymorphisms may contribute to the disease-associated cytokine imbalance. However, to the best of our knowledge, there is no existing meta-analysis concerning an association of the cytokine gene functional polymorphisms with the susceptibility / severity of ARF/RHD. Aims To investigate the potential association between cytokine gene functional polymorphisms of TNF-α, TGF-β, IL-10, IL-6 and IL-1β and the susceptibility and severity of ARF/RHD. Methods Comprehensive and structured search on Pubmed/Medline, Embase, EBSCO, and Cochrane Central Register of Controlled Trials was performed. Statistical analyses were performed using STATA. First, we performed direct pairwise meta-analysis. Then, a network meta-analysis was performed with the consistency model to compare the genetic models of different cytokine gene polymorphisms. Results Evidence derived from the meta-analysis of 24 retrospective cohort and case-control studies identified that elevated serum levels of TNF-α have been observed in ARF cases, occurring as a result of a SNP (-308G&amp;gt;A) in the promoter site of the TNF-α gene. Our results also suggest that IL-1β (-511) C/T polymorphism, TGF-β1 [rs1800469], and IL-1β [rs2853550] single nucleotide polymorphisms (SNPs) contributed to the susceptibility of ARF/RHD. Egger’s test did not demonstrate significant asymmetry in the dominant. Conclusion In summary, the polymorphism model increased the risk of RHD in the dominant genetic model, recessive genetic model, homozygote model and allelic genetic model among non-Asians while, recessive genetic model and homozygote model among Asians.

Vulnerability biomarkers for mental illness and suicide risk: Regards for the development of pharmacological and psychological therapies

• The result of the administered Multivariate Analysis showed the relationship between the independent variables genetic polymorphism, environmental domains (DMA) and social relations domain (DRS) and the dependent variables, psychological domain, physical domain and risk of suicide. • The first data table refers to the analysis of the intersections of the independente variables (fixed factors) of the 5HTT, TNF, IL-10 polymorphisms, social relationship domain (DRS) and environmental domain (DMA). A statistically significant difference was found. The last four lines indicate intersections with a tendency towards significance, whereas in the fourth line, the results indicate that in the interaction between DRS, DMA and IL-10 the variance becomes significant, that is, with a low propensity to occur by chance. • The same progression that tends to be significant is expressed in the interaction between DRS,DMA and IL-10. The interaction of these three variables, especiallywith regard to the quality of the possible outcomes of the dependent variables, points to a statistically significant difference for the risk of suicide. • The IL - 10 gene seems to increase the risk of suicide and could be configured as a diathesis factor in screening for the detection of a risk factor for suicide. According to the diathesis-stress model, some individuals may have a certain underlying vulnerability (diathesis) that can be environmental or biological, such as a childhood trauma or a genetic predisposition. Hence, it is important to understand the epigenetic factors and the presence of biomarkers related to mental illness and suicide risk. The present study aimed to evaluate if the presence of rs1800871 (IL- 10), rs2020933 (5-HTT) and rs1800629 (TNF – α) polymorphisms express different outcomes in terms of physical, psychological health and quality of life, considering the relations among them and the social environment, through observation of the psychological, physical, environment domains and the quality of social relations. A multivariate analysis (MANOVA) of the data was conducted, in which 481 participants were assessed through the instruments Quality of Life Brief Questionnaire (QOL – brief), Beck's Scale of Suicide Ideation (BSI) and the Mini International Neuropsychiatric Interview (MINI 5.5.0). The participants´ DNA was collected through a saliva sample of the oral mucosa. From the studied sample, 306 participants had mental disorder (MD) with no history of suicide attempt (HSA), 145 showed MD with HSA and 175 participants. A statistically significant difference (0.001 and 0.004) was found in the interaction of two factors, namely the social relationships domain and the presence of the IL- 10 polymorphism, leading to increased suicide risk and lower levels of quality of life in the physical domain. The interaction between the rs1800871 (IL-10) polymorphism and lower levels of quality of life in the environment and social environment domains appears to be related to a worse perception of physical health and a higher risk of suicide, which highlights the epigenetic influence for both physical and mental illness.

Elucidating the Genetic Factors Contributing Towards Susceptibility and Severity of Covid 19

COVID-19 or SARS-CoV-2 or 2019-nCov is a pandemic disease that occurred in December 2019 in Wuhan, Hubei Province of China. It was first transmitted from the animal host to a human source, after which it followed human-human transmission and spread exponentially worldwide. Various countries have fallen prey to this virus, but there are certain countries or populations, which have been more affected by this than others. Moreover, the demographics of transmission and affected individuals are also variable from country-country. The purpose of this article is to highlight the non-modifiable risk factors for COVID-19 and their analysis in various populations affecting their susceptibility. Besides age, gender, and blood group, two major genetic factors associated with this disease are discussed here, including the potential of IL-6, in causing chronic disease conditions and the rs1800795 G/C-174 IL-6 polymorphism in the IL-6 gene and with the potential role of ACE-2 receptor in viral transmission and pathogenicity with its protective and disease-causing variants.

Association of IL4 rs2070874, FoxP3 rs3761548 Polymorphisms with Keratoconus in Algeria.

Purpose The aim of this case–control study was to determine the impact of environmental factors on the predisposition to develop keratoconus in a sample of Western Algerian population. Subsequently, we were interested in the implication of two single nucleotide polymorphisms (SNPs) IL4 rs2070874 and FOXP3 rs3761548, previously described as contributing to the occurrence of allergy, in the development of keratoconus.MethodsThe study included 70 unrelated KC cases and 70 controls originating from Western Algeria. DNA genotyping was done using predesigned probe-based allelic discrimination TaqManⓇ assays. Allele and genotype frequencies were compared between the cases and controls by Chi-square test and odds ratios with 95% confidence intervals.ResultsA significant association between risk factors such as family history, atopy, eye rubbing, and the development of keratoconus was found in our sample. Smoking would provide a protective effect against the pathology. No statistically significant differences were found in the allele and genotype frequencies between cases and controls neither for IL4 rs2070874 nor for FOXP3 rs3761548.ConclusionOur study provides, for the first time, a clear demonstration of the absence of association of the allergy-associated IL4 and FOXP3 polymorphisms with KC in a sample from Western Algerian population.