IL-10 Gene Promoter Research Articles

Legionella pneumophila-induced IκBζ-dependent expression of interleukin-6 in lung epithelium

Severe community- and hospital-acquired pneumonia is caused by Legionella pneumophila. Lung airway and alveolar epithelial cells comprise an important sentinel system in airborne infections. Although interleukin (IL)-6 is known as a central regulator of the immune response in pneumonia, its regulation in the lung is widely unknown. Herein, we demonstrate that different L. pneumophila strains induce delayed expression of IL-6 in comparison with IL-8 by human lung epithelial cells. IL-6 expression depended, at early time points, on flagellin recognition by Toll-like receptor (TLR)5, activity of mitogen-activated protein kinase/extracellular signal-regulated kinase kinase (MEK)1 and p38 mitogen-activated protein (MAP) kinase, and, at later time points, on the type-IV secretion system. In the same manner, but more rapidly, the recently described transcription factor IκBζ was induced by Legionella infection and, binding to the nuclear factor (NF)-κB subunit p50 - recruited to the il6 promoter together with CCAAT-enhancer-binding protein β and phosphorylated activator protein-1 subunit cJun. Similarly, histone modifications and NF-κB subunit p65/RelA appeared at the iκbζ and subsequently at the il6 gene promoter, thereby initiating gene expression. Gene silencing of IκBζ reduced Legionella-related IL-6 expression by 41%. Overall, these data indicate a sequence of flagellin/TLR5- and type IV-dependent IκBζ expression, recruitment of IκBζ/p50 to the il6 promoter, chromatin remodelling and subsequent IL-6 transcription in L. pneumophila-infected lung epithelial cells.

Association of interleukin-10 gene polymorphisms with breast cancer in a Chinese population

BackgroudInterleukin-10(IL-10) is a multifunctional cytokine with both immunosuppressive and antiangiogenic functions. Polymorphisms in the IL-10 gene promoter genetically determine interindividual differences in IL-10 production. This study was performed to determined whether polymorphisms in the IL-10 gene promoter were associated with breast cancer in a Chinese Han population.MethodsWe genotyped 315 patients with breast cancer and 322 healthy control subjects for -1082A/G, -819T/C and -592A/C single nucleotide polymorphisms in the promoter region of the IL-10 gene by polymerase chain reactionerestriction fragment length polymorphism (PCR-RFLP).ResultsThere were no significant differences in genotype, allele, or haplotype frequencies in all three loci between patients and healthy controls. Analysis of breast cancer prognostic and predictive factors revealed that the -1082AA genotype was associated with a significantly increased risk of lymph node (LN) involvement (P = 0.041) and larger tumor size (P = 0.039) at the time of diagnosis. Furthermore, in the haplotype analysis of IL-10 gene, we found that patients carrying ATA haplotype were in higher LN involvement (p = 0.022) and higher tumor stage(p = 0.028) of breast cancer at the time of diagnosis compared with others.ConclusionsOur findings suggest that IL-10 promoter polymorphisms participate in the progression of breast cancer rather than in its initial development in Chinese Han women.

LPS-induced IL-8 activation in human intestinal epithelial cells is accompanied by specific histone H3 acetylation and methylation changes

BackgroundThe release of LPS by bacteria stimulates both immune and specific epithelial cell types to release inflammatory mediators. It is known that LPS induces the release of IL-8 by intestinal mucosal cells. Because it is now emerging that bacteria may induce alteration of epigenetic patterns in host cells, we have investigated whether LPS-induced IL-8 activation in human intestinal epithelial cells involves changes of histone modifications and/or DNA methylation at IL-8 gene regulatory region.ResultsRT-PCR analysis showed that IL-8 mRNA levels rapidly increase after exposure of HT-29 cells to LPS. DNA demethylating agents had no effects on IL-8 expression, suggesting that DNA methylation was not involved in IL-8 gene regulation. Consistently we found that 5 CpG sites located around IL-8 transcription start site (-83, -7, +73, +119, +191) were unmethylated on both lower and upper strand either in LPS treated or in untreated HT-29 cells, as well as in normal intestinal mucosa.Conversely, pretreatment of HT-29 cells with deacetylase inhibitors strengthened the LPS-mediated IL-8 activation. Inhibitors of histone deacetylases could induce IL-8 mRNA expression also in the absence of LPS, suggesting that chromatin modifications could be involved in IL-8 gene regulation. Chromatin immunoprecipitation analyses showed that, concurrently with IL-8 activation, transient specific changes in H3 acetylation and H3K4, H3K9 and H3K27 methylation occurred at IL-8 gene promoter during LPS stimulation. Changes of H3-acetyl, H3K4me2 and H3K9me2 levels occurred early, transiently and corresponded to transcriptional activity, while changes of H3K27me3 levels at IL-8 gene occurred later and were long lasting.ConclusionThe results showed that specific chromatin modifications occurring at IL-8 gene, including histone H3 acetylation and methylation, mark LPS-mediated IL-8 activation in intestinal epithelial cells while it is unlikely that DNA methylation of IL-8 promoter is directly involved in IL-8 gene regulation in these cells.

FC25 IL-18 promoter variations at position -607 C/A is associated with individuals susceptibility to Basal Cell Carcinoma

Introduction Human keratinocytes are the main source of pro-IL-18. These cells are capable of producing biologically active form of the cytokine. Objectives IL-18 potentially induces IFN-γ production in response to a variety of stimuli and subsequently plays a role in numerous types of skin disorders by promoting inflammation as well as deviation from Th2 to Th1 response. IL-18 and Th1 cytokines have a duel effect against and, simultaneously, in favor of cancer progression. A ‘C to A transition’ at position -607 in IL-18 gene has been recently reported to affect activity of the gene promoter. Aims We aimed to evaluate association of IL-18 gene promoter polymorphism at position -607 C/A with genetic susceptibility to BCC. Methods 97 patients with BCC and 194 matched healthy individuals with no history of cancer or autoimmune disease (mean age: 59.96±10.73) recruited to the study. PCR with Allele specific primer (ASP) was performed to determine genotypes. Results The frequencies of CC, CA and AA genotype in patients and control group were respectively 25.8% vs 38.6%, 60.8% vs 45.4% and 13.4% vs 16%. Statistical analysis revealed that CC genotype frequency in patients was significantly higher than controls (P=0.04, OR=1.82, 95% CI for OR 1.02–3.23). No significant differences was observed in the frequencies of the alleles between two groups (P=0.29). Conclusion Our data suggest that significant increase in CC genotype at locus -607C/A in IL-18 gene is associated with susceptibility to BCC in Iranian population, most likely by promoting IL-18 production at the tumor microenvironment. Key Words: Basal Cell Carcinoma, Interlukin-18, Polymerase Chain Reaction (PCR), Polymorphism

Interleukin 10 gene polymorphism in Iranian patients with multiple sclerosis.

IL-10 suppresses several activities of the immune response by inhibition of Th1 and Th2 cells. We studied 110 Iranian patients with clinically definite multiple sclerosis (MS) and 100 ethnic and age matched controls. Three single-nucleotide polymorphisms in the proximal region of IL-10 promoter gene (-1082/-819/-592) were analysed by amplification refractory mutation system (ARMS) and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methods. The -1082 (G/A), -819 (T/C) and -592 (A/C) genotypes were similarly distributed between MS patients and the controls. There was no statistically significant difference in the allelic and genotype distribution between patients and controls. In addition, gender, course and progression index did not reveal any statistically significant differences in the allele and genotype distribution of IL-10 polymorphisms. As a non-European patient population, according to our results, IL10 polymorphism is not associated with MS and its subtypes nor influences the disease progression.

−607 C/A polymorphism in the promoter of IL-18 gene is associated with 2 h post-loading plasma glucose level in Chinese

The purpose of this study is to find out whether the -607 C/A polymorphism in IL-18 gene promoter will affect serum IL-18 concentrations and glucose metabolism in Chinese subjects. In 232 patients with impaired glucose regulation (IGR) or type 2 diabetes and 212 subjects of normal glucose regulation (NGR), -607 C/A polymorphism was analyzed by polymerase chain reaction with sequence specific primers. Serum IL-18 concentrations were determined by ELISA in 200 subjects. Compared with subjects with NGR, those with type 2 diabetes and IGR had significant higher IL-18 concentrations [114.4 (92.9-149.2) and 102.1 (67.5-138.2) vs. 77.3 (53.8-107.8) pg/ml, P=0.0026 and P<0.0001, respectively]. A significantly higher proportion of A/A genotype of -607 C/A polymorphism presented in patients with type 2 diabetes compared with subjects of NGR (23.8% vs. 10.9%, P=0.005). Subjects with an A/A genotype also had higher 2h post-loading plasma glucose (2h-PPG) compared with C/A and C/C genotypes even after adjustments of age, sex and BMI [8.94 (7.55-12.3) vs. 7.80 (6.00-9.87) and 7.23 (5.66-8.99) mmol/l, P both<0.05]. Multiple linear regression revealed that BMI (P<0.0001) and 2h-PPG (P=0.019) were independently associated with IL-18 concentrations. In conclusion, subjects with IGR or type 2 diabetes had significantly higher concentrations of IL-18 than those with NGR. Genotype A/A of IL-18 gene promoter -607 C/A polymorphism was associated with higher prevalence of type 2 diabetes and 2h post-loading plasma glucose level.

Interleukin-10 Gene Polymorphisms Influence Susceptibility to Cachexia in Patients with Low-Third Gastric Cancer in a Chinese Population

Interleukin (IL)-10 is a pleiotropic cytokine that can both stimulate and suppress the immune response. Previous studies have reported that IL-10 production was significantly elevated in cachectic patients, and it has been confirmed that polymorphisms of the IL10 gene could influence its expression. Therefore, we designed this study to investigate whether polymorphisms of the IL10 gene were associated with cachexia in patients with low-third gastric cancer in a Chinese population. 190 patients with low-third gastric cancer were included in this study. The serum levels of IL-10 were measured by radioimmunoassay. The single nucleotide polymorphisms (SNPs) at positions -1082A/G, -819T/C, and -592A/C in the IL10 gene promoter were analyzed using polymerase chain reaction (PCR) restriction fragment length polymorphism (PCR-RFLP). The serum levels of IL-10 were significantly higher in patients with cachexia than in those without (Z = -10.66, p < 0.001). Single SNP analysis showed that the frequency of the IL10 -1082G allele was increased in patients with cachexia (p = 0.02). The -1082AG and -819CC genotypes were observed to be associated with an increased risk of cachexia. In a logistic regression analysis adjusted for actual weight and carcinoma stage, the -1082AG genotype was associated with an odds ratio (OR) of 2.45 (95% CI 1.21, 4.96; p = 0.01), and the -819CC genotype was associated with an OR of 3.70 (95% CI 1.20, 11.39; p = 0.02) for cachexia. Furthermore, haplotype analysis of the -1082A/G, -819T/C, and -592A/C SNPs revealed that at least five haplotypes (ATA, ACC, GCC, ACA, and ATC) were present in this Chinese population, and the -1082G/-819C/-592C (GCC) haplotype was associated with a significantly increased risk of cachexia as compared with the ATA haplotype (OR = 2.42; 95% CI 1.17, 5.00; p = 0.02). Our results indicate that genetic polymorphisms of IL-10 may influence susceptibility to cachexia in patients with low-third gastric cancer in this Chinese population.

ATF3-Mediated Epigenetic Regulation Protects against Acute Kidney Injury

A variety of stress stimuli, including ischemia-reperfusion (I/R) injury, induce the transcriptional repressor ATF3 in the kidney. The functional consequences of this upregulation in ATF3 after renal I/R injury are not well understood. Here, we found that ATF3-deficient mice had higher renal I/R-induced mortality, kidney dysfunction, inflammation (number of infiltrating neutrophils, myeloperoxidase activity, and induction of IL-6 and P-selectin), and apoptosis compared with wild-type mice. Furthermore, gene transfer of ATF3 to the kidney rescued the renal I/R-induced injuries in the ATF3-deficient mice. Molecular and biochemical analysis revealed that ATF3 interacted directly with histone deacetylase 1 (HDAC1) and recruited HDAC1 into the ATF/NF-kappaB sites in the IL-6 and IL-12b gene promoters. The ATF3-associated HDAC1 deacetylated histones, which resulted in the condensation of chromatin structure, interference of NF-kappaB binding, and inhibition of inflammatory gene transcription after I/R injury. Taken together, these data demonstrate epigenetic regulation mediated by the stress-inducible gene ATF3 after renal I/R injury and suggest potential targeted approaches for acute kidney injury.

Involvement of capsular polysaccharide via a TLR2/NF-κB pathway in Vibrio vulnificus-induced IL-8 secretion of human intestinal epithelial cells

In a previous study, we reported that a wbpP gene mutation in Vibrio vulnificus was significantly impaired in its ability to synthesize surface capsular polysaccharide (CPS). In this study, we evaluated the functions of the V. vulnificus capsular polysaccharide on interleukin (IL)-8 production, as well as its underlying mechanisms in human intestinal epithelial cells. The CPS-defective wbpP mutant induced significantly lower levels of IL-8 production, IL-8 gene promoter activation and NF-kappaB activity in INT-407 cells than was noted with the wild-type or wbpP-complemented V. vulnificus. The expression levels of Toll-like receptor (TLR)2 mRNA and protein were also found to be lower in INT-407 cells infected with the CPS-defective wbpP mutant than in those cells infected with the wild-type or the wbpP-complemented strains. Additionally, the treatment of INT-407 cells with anti-TLR2 antibody proved to significantly block IL-8 production and NF-kappaB minimal promoter activity induced by the wild-type or the wbpP-complemented strains. Furthermore, purified V. vulnificus CPS was found to significantly induce IL-8 production and NF-kappaB activation, both of which were inhibited upon the addition of the anti-TLR2 antibody. Taken together, these results demonstrate that V. vulnificus capsular polysaccharide is involved in the induction of IL-8 production of human intestinal epithelial cells via a TLR2/NF-kappaB-dependent pathway.

Functional relevance of IL-10 promoter polymorphisms for sepsis development

The induced production of proinflammatory and anti-inflammatory cytokines is considered important for the development of sepsis and its sequelae. Polymorphisms in the IL-10 gene promoter could influence its expression and sepsis susceptibility. Results obtained by Dr Ling and colleagues demonstrated that the -1082A allele was significantly associated with lower lipopolysaccharide-induced IL-10 production in an allele-dose-dependent fashion. They also showed that this polymorphism was significantly associated with sepsis development after major trauma. These and other research data clearly demonstrated that the -1082 A/G polymorphism in the IL-10 gene promoter has an important impact on susceptibility of sepsis and sepsis outcome.

Association between IL-18gene polymorphisms and biopsy-proven giant cell arteritis

IntroductionThe objective was to investigate the potential implication of the IL18 gene promoter polymorphisms in the susceptibility to giant-cell arteritis (GCA).MethodsIn total, 212 patients diagnosed with biopsy-proven GCA were included in this study. DNA from patients and matched controls was obtained from peripheral blood. Samples were genotyped for the IL18-137 G>C (rs187238), the IL18-607 C>A (rs1946518), and the IL18-1297 T>C (rs360719) gene polymorphisms with polymerase chain reaction, by using a predesigned TaqMan allele discrimination assay.ResultsNo significant association between the IL18-137 G>C polymorphism and GCA was found. However, the IL18 -607 allele A was significantly increased in GCA patients compared with controls (47.8% versus 40.9% in patients and controls respectively; P = 0.02; OR, 1.32; 95% CI, 1.04 to 1.69). It was due to an increased frequency of homozygosity for the IL18 -607 A/A genotype in patients with GCA (20.4%) compared with controls (13.4%) (IL18 -607 A/A versus IL18 -607 A/C plus IL18 -607 C/C genotypes: P = 0.04; OR, 1.59; 95% CI, 1.02 to 2.46). Also, the IL18-1297 allele C was significantly increased in GCA patients (30.7%) compared with controls (23.0%) (P = 0.003; OR, 1.48; 95% CI, 1.13 to 1.95). In this regard, an increased susceptibility to GCA was observed in individuals carrying the IL18-1297 C/C or the IL18-1297 C/T genotypes compared with those carrying the IL18-1297 T/T genotype (IL18-1297 C/C plus IL18-1297 T/C versus IL18-1297 T/T genotype in GCA patients compared with controls: P = 0.005; OR, 1.61; 95% CI, 1.15 to 2.25). We also found an additive effect of the IL18 -1297 and -607 polymorphisms with TLR4 Asp299Gly polymorphism. The OR for GCA was 1.95 for combinations of genotypes with one or two risk alleles, whereas carriers of three or more risk alleles have an OR of 3.7.ConclusionsOur results show for the first time an implication of IL18 gene-promoter polymorphisms in the susceptibility to biopsy-proven GCA. In addition, an additive effect between the associated IL18 and TLR4 genetic variants was observed.

Relationship between IL-10 gene promoter polymorphisms and outcome of hepatitis B virus infection

Relationship between IL-10 gene promoter polymorphisms and outcome of hepatitis B virus infection

Lack of an association between a functional polymorphism in the interleukin-6 gene promoter and breast cancer risk: a meta-analysis involving 25,703 subjects

The association between a single-nucleotide polymorphism (SNP) -174G > C (rs1800795) located in the IL-6 gene promoter and breast cancer risk is still controversial and ambiguous. We performed in this study a more precise estimation of the relationship by meta-analyzing the currently available evidence from literature. A total of 11 publications containing 12 studies including 10,137 cases and 15,566 controls were identified. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of association in the codominant model, dominant model, and recessive model. When all the studies were pooled into the meta-analysis, there was no evidence showing a significant association between -174G > C and breast cancer risk (for CC vs. GG: OR = 1.024, 95% CI: 0.935-1.121; for GC vs. GG: OR = 1.008, 95% CI: 0.946-1.073; for dominant model: OR = 0.980, 95% CI: 0.857-1.121; and for recessive model: OR = 1.027, 95% CI: 0.944-1.117). In the subgroup analyses by ethnicity, no significant associations were observed in any genetic models. In summary, the present meta-analysis suggests that the functional polymorphism -174G > C within the IL-6 gene promoter is not associated with breast cancer risk. Identifying a unique SNP as a breast cancer risk predictor remains a very challenging task.

Interleukin 10 Gene Polymorphisms and Development of Post Kala-Azar Dermal Leishmaniasis in a Selected Sudanese Population

Background: Post kala-azar dermal leishmaniasis (PKDL) is a cutaneous form of disease that develops at variable times after individuals have received treatment for clinical visceral leishmaniasis (VL). The study aimed to investigate the possible role of interleukin 10 (IL-10) and development of PKDL. Methods: 77 families composed of 41 complete case-parent trios and 36 case-parent pairs from the Masalit ethnic group were genotyped for 3 IL10 promoter polymorphisms: -1082A/G, -819C/T and -592C/A. Results: Single point analysis using the transmission disequilibrium test showed no evidence of association between any of these IL10 promoter single nucleotide polymorphisms (SNPs) and development of PKDL. Haplotype analysis performed using TRANSMIT showed borderline significance between PKDL and the haplotype AA across -592C/A and -1082A/G (p = 0.053). Haplotypes GCC (0.33) and ATA (0.30) were the common haplotypes in this Sudanese population. Allele frequencies for the 3 SNPs differed significantly in Sudan compared to other African (Gambian, Malawian, YRI) populations. Conclusion: There is no evidence for an association between 3 SNPs in the IL10 gene promoter and susceptibility to PKDL in the Masalit ethnic group in Sudan, although some evidence for haplotype association was observed.

Il6 gene promoter polymorphism (-174G/C) influences the association between fat mass and cardiovascular risk factors

During the last decades, the prevalence of obesity has increased rapidly among young people. A polymorphism in the promoter region of the IL6 gene (-174G/C), has been previously reported to be involved in obesity and metabolic syndrome development. Therefore, the aim of the study was to examine whether the IL6-174G/C polymorphism influence the association of body fat with low-grade inflammatory markers and blood lipids and lipoproteins in Spanish adolescents. 504 Spanish adolescents participating in the AVENA study were genotyped for the-174G/C polymorphism of the IL6 gene. Anthropometric and body composition measurements were taken and blood samples were collected for plasma molecules determinations. No differences between genotypes were observed in anthropometric values, body composition measurements and plasma markers concentration. Physical activity level differ between genotypes with subjects carrying the C allele of the polymorphism being significantly (p<0.05) more active than GG subjects. The association between body fat mass and plasma glucose was influenced by the -174G/C polymorphism of the IL6 gene. Subjects carrying the C allele of the mutation seem to have higher values of lipoprotein (a) and C-reactive protein as their percentage of body fat mass increase. Our results suggest that this promoter polymorphism influences the association between adiposity and some plasma markers.

Monocyte-Derived Interleukin-10 Depresses the Bordetella pertussis - Specific Gamma Interferon Response in Vaccinated Infants

Antigen-specific gamma interferon (IFN-gamma) has been demonstrated to participate in protection against Bordetella pertussis infection. Circulating mononuclear cells from B. pertussis-infected and from pertussis-vaccinated infants secrete high amounts of IFN-gamma after in vitro stimulation by B. pertussis antigens, but with a large variation in the secreted IFN-gamma levels between individuals. We show here that the inhibition of the specific IFN-gamma response can be at least partially attributed to IL-10 secretion by monocytes. This IL-10 secretion was not associated with polymorphisms at positions -1082, -819, and -592 of the IL-10 gene promoter, suggesting that other genetic or environmental factors affect IL-10 expression and secretion.

Hyperactivated NF-κB and AP-1 Transcription Factors Promote Highly Accessible Chromatin and Constitutive Transcription across the Interleukin-6 Gene Promoter in Metastatic Breast Cancer Cells

Interleukin-6 (IL-6), involved in cancer-related inflammation, acts as an autocrine and paracrine growth factor, which promotes angiogenesis, metastasis, and subversion of immunity, and changes the response to hormones and to chemotherapeutics. We explored transcription mechanisms involved in differential IL-6 gene expression in breast cancer cells with different metastatic properties. In weakly metastatic MCF7 cells, histone H3 K9 methylation, HP1 binding, and weak recruitment of AP-1 Fra-1/c-Jun, NF-kappaB p65 transcription factors, and coactivators is indicative of low chromatin accessibility and gene transcription at the IL-6 gene promoter. In highly metastatic MDA-MB231 cells, strong DNase, MNase, and restriction enzyme accessibility, as well potent constitutive transcription of the IL-6 gene promoter, coincide with increased H3 S10 K14 phosphoacetylation and promoter enrichment of AP-1 Fra-1/c-Jun and NF-kappaB p65 transcription factors and MSK1, CBP/p300, Brg1, and Ezh2 cofactors. Complementation, silencing, and kinase inhibitor experiments further demonstrate involvement of AP-1 Fra-1/c-Jun and NF-kappaB p65/RelB members, but not of the alpha estrogen receptor in promoting chromatin accessibility and transcription across the IL-6 gene promoter in metastatic breast cancer cells. Finally, the natural withanolide Withaferin A was found to repress IL-6 gene transcription in metastatic breast cancer cells upon dual inhibition of NF-kappaB and AP-1 Fra-1 transcription factors and silencing of IL-6 promoter chromatin accessibility.

Interleukin‐10 promoter polymorphisms in hepatitis C patients with and without Schistosoma mansoni co‐infection

Interleukin (IL-10) plays a major role in chronic hepatitis C virus (HCV) disease pathogenesis, in particular in Schistosoma mansoni (S. mansoni) co-infected patients. Given that interindividual variations in IL-10 production are influenced by functional polymorphisms in the IL-10 gene promoter, we determined the frequencies of common (-1082, -819 and -592) IL-10 promoter polymorphisms in chronic HCV patients with and without S. mansoni co-infection and healthy controls, and investigated their association with the degree of histological activity index (HAI) and response to interferon-ribavirin therapy. Genomic DNA from 99 patients and 62 healthy controls, born in the same geographical hyperendemic area, was studied by the polymerase chain reaction, followed by restriction enzyme digestion. Sera were assessed for S. mansoni antibodies. The frequencies of IL-10 polymorphisms at positions -1082, -819 and -592 from the transcription start site were comparable between HCV patients and controls, as well as between HCV mono-infected and either S. mansoni co-infected patients or controls. The grade of inflammation and the stage of fibrosis showed no association with IL-10 polymorphisms. The frequencies of S. mansoni co-infection and IL-10 genotypes/haplotypes were insignificantly different between non-responders and responders to combination therapy. No effect of other factors like age, gender, HAI group scores and serum alanine aminotransferase and aspartate aminotransferase levels was observed on response to therapy in our patients. Our findings suggest that common IL-10 (-1082, -819 and -592) genotypes/haplotypes do not influence the degree of HAI and response to combination therapy or susceptibility to HCV infection with and without S. mansoni co-infection.

OL-051 Regulatory polymorphisms in the IL-10 gene promoter and HBV-related acute liver failure in the Chinese population

OL-051 Regulatory polymorphisms in the IL-10 gene promoter and HBV-related acute liver failure in the Chinese population

Relationship between IL-10 promoter gene polymorphisms and the susceptibility to endometriosis

The purpose of this study was to investigate the relationship between IL-10 promoter gene polymorphism and the susceptibility to endometriosis (EMs) in Chinese population. Amplification refractory mutation system polymerase chain reactions (ARMS-PCR) and DNA sequencing were performed to detect polymorphism of -1082G/A site and PCR-RFLP was used to determine the genotypes in -819T/C and -592A/C sites. One hundred and nineteen Chinese women with different stage EMs and 120 controls were employed in this study. Although there were no significant differences in the polymorphism of -1082 site between two groups (P>0.05), the frequencies of -819C, -592C alleles and -819 CC+TC, -592 CC+AC genotypes were significantly increased in EMs patients compared with the controls (P<0.05). The frequencies of -819C, -592C alleles and -819 CC+TC, -592 CC+AC genotypes were significantly increased in III-IV EMs patients compared with I-IIMs or controls (P<0.01). This suggests that polymorphisms of IL-10-819 (T/C) and -592 (A/C) may be associated with the susceptibility to EMs in Chinese population.