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.

No abstract

No abstract