Genetic factors predispose individuals to Behçet's disease (BD) and periodontal disease. IL-1 has been implicated in the pathogenesis of both BD and periodontal disease. The relationship between periodontitis and pathogenesis of BD has not yet been determined. Since IL-1 has been implicated in the pathogenesis of both BD and periodontal disease, we aimed to investigate the possible relation of the periodontal scores and SNPs of IL-1alpha-889C/T, IL-1beta-511C/T, and IL-1beta+3962T/C with BD compared to healthy controls (HC) and recurrent aphtous stomatitis (RAS). A total of 155 Turkish individuals were enrolled in this study. The periodontal status of all subjects was evaluated according to the WHO community periodontal index of treatment needs. For genotyping, CTS-PCR-SSP was employed. IL-1alpha-889C allele was significantly higher in BD patients (p = 0.03) and RAS (p = 0.02) compared to HC. The frequency of IL-1beta+3962T allele was significantly higher in RAS patients compared to HC (p = 0.015). Male gender (p = 0.04), age (p = 0.02) and carrying IL-1beta-511T allele (p = 0.01) were found to be a significant risk factors for higher periodontal scores in Turkish population. We can speculate that susceptibility to the development of periodontal disease could be influenced by IL-1 SNPs. Periodontitis-induced autoinflammatory response also may play a role in the development/severity of BD and RAS via IL-1 gene alteration.
Mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS) is a common medically intractable epilepsy syndrome. Although pathogenesis of HS still remains highly controversial, genetics may play a role as a predisposing factor. Previous evidence in a Japanese population revealed that the homozygotes for allele T at position -511 of the interleukin (IL)-1β gene promoter region (IL-1β-511 T/T) confers susceptibility to the development of HS. However, whether this polymorphism has an effect on IL-1β levels in MTLEHS patients was not demonstrated. This study aimed to analyze the distribution of this particular polymorphism in a group of Turkish HS patients and correlate the polymorphism with IL-1β secretion from the lymphocytes, thus revealing a functional role for IL-1β in the etiopathogenesis of HS. A single base pair polymorphism at position –511 in the promoter region of the IL-1β gene was analyzed. The spontaneous and 1 ng/mL lipopolysaccharidestimulated production of IL-1β by peripheral blood mononuclear cells after 4 and 24 h of incubation were measured by ELISA method. The heterozygous type (–511 C/T) was the most common genotype. There was no difference in frequency of allele –511 T between patients and controls. Analysis of IL-1β levels, genotype and allele distributions showed no significant difference among the groups (P>0.05). Nevertheless, it was seen that patients who carry a T allele at position -511 of the IL-1β gene had increased IL-1β levels. T-allele carriage may be important. Only IL-1β secretion from the lymphocytes has been assessed in this study. Considering the importance of IL-1β in the etiopathogenesis of HS, further studies are needed to evaluate locally produced IL-1β levels.
Subacute sclerosing panencephalitis (SSPE) is a progressive and fatal disease caused by reactivation of a mutated measles virus in brain tissue. The process of reactivation is yet to be elucidated. In this study, the possible roles of the Th1 (interleukin [IL]-12, interferon [IFN]-γ) and the Th17 axis (IL-23, IL-17, IL-22), particularly of IL-17, in the pathogenesis of SSPE were investigated. Briefly, mononuclear cells from SSPE patients were stimulated using measles virus peptide, and the release of IL-12, IL-23, IL-22, IFN-γ, and IL-17 cytokines was measured using enzyme-linked immunosorbent assay and/or enzyme-linked immunosorbent spot assay (ELISpot). We found that in comparison to the mononuclear cells obtained from healthy donors, cells from SSPE patients exhibited increased levels of IL-12, IL-23, IL-17, IL-22, and IFN-γ cytokines in response to measles virus stimulation. However, the same result was not obtained with cytomegalovirus and phytohemagglutinin. Using flow cytometry, mononuclear cells obtained from SSPE patients and healthy controls were also analyzed for the presence of intracellular IL-17 in response to measles virus stimulation. On stimulation, the number of IL-17-positive cells were found to be higher among mononuclear cells obtained from the patients. In addition, the numbers of IL-17- and IFN-γ-positive cells were significantly increased in SSPE patients. In conclusion, this study demonstrates that both the IL-12/IFN-γ and the IL-23/IL-17/IL-22 pathways are functionally abnormal in SSPE pathogenesis. Targeting these pathways and their specific pro-inflammatory mediator production may provide a new strategy to suppress SSPE development.
Background The etiology of rheumatoid arthritis (R.A.), an autoimmune, polygenic, inflammatory disease, has not yet been clarified despite the intense research1. In addition to its more commonly known metabolic effects such as those associated with calcium homeostasis, vitamin D has, in general, suppressive effects on the immune system, especially on T helper cell function. T cells are critical in the development of autoimmune reactions and autoimmune diseases. Low vitamin D levels have been associated with the risk of development of R.A., an autoimmune disease2. Vitamin D functions are mainly accomplished through vitamin D receptor (VDR). Several VDR gene polymorphisms have been described, and they may affect the function of vitamin D3. Objectives The aim of this study is to detect whether the frequence of 4 VDR gene polymorphisms (ApaI, BsmI, FokI ve TaqI) differ in R.A. patients with respect to healthy controls. Whether these polymorphisms cause a difference in several clinical activation parameters (ESR, CRP, RF, DAS28 and Sharp score) of the patients was also determined. Methods Study groups consisted of a R.A. group of 100 patients and 100 healthy controls. ApaI, BsmI, FokI and TaqI gene polymorphisms were studied by using polymerase chain reaction. Results Statistically significant difference was only detected in only one of the 4 VDR gene polymorphisms, the BsmI gene, in the study. BB genotype of BsmI gene was more common in the R.A. group with respect to controls (p<0.05, odds ratio: 3.6, confidence interval: 1,4-9,7, chi2:1,03). There was no significant difference in the other 3 VDR genes. Within the clinical features studied, only CRP showed statistically significant difference in patients with any VDR gene polymorphism. High CRP was determined to be significantly more common in the R.A. patients with TaqI polymorphism with respect to the other patients (p=0.025). Conclusions In this study, no significant correlation was found between VDR gene polymorphisms and RA activity. Statistically significant difference was only detected in only one of the 4 VDR gene polymorphisms, the BsmI gene. BB genotype of BsmI gene was more common in the R.A. group. BsmI polymorphism may be a preventing feature of R.A development. References Seldin MF, Amos CI, Ward R, Gregersen PK. The genetics revolution and the assault on rheumatoid arthritis. Arthritis Rheum. Jun 1999;42(6):1071-1079. Cantorna MT, Mahon BD. Mounting evidence for vitamin D as an environmental factor affecting autoimmune disease prevalence. Exp Biol Med (Maywood). Dec 2004;229(11):1136-1142. Guo SW, Magnuson VL, Schiller JJ, Wang X, Wu Y, Ghosh S. Meta-analysis of vitamin D receptor polymorphisms and type 1 diabetes: a HuGE review of genetic association studies. Am J Epidemiol. Oct 15 2006;164(8):711-724. Disclosure of Interest None Declared
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