Evaluation of the effects of chronic periodontitis on TLR-2 and TLR-4 gene expression in gingival tissues

In periodontal diseases, pathogen discrimination by the immune system is an essential factor for triggering host responses. The Toll-like receptor family is responsible for recognition of evolutionarily conserved microbial structures like bacterial lipopolysaccharide [LPS] and activates signaling pathways that eventually lead to immune responses. The aim of the present study was to use real-time PCR to compare TLR-2 and TLR-4 gene expression levels in diseased sites and healthy sites of gingival tissue from periodontitis patients. Gingival biopsies were harvested from healthy sites [BOP- and PD /= 5mm] of 20 patients with moderate to severe chronic periodontitis. RNA was extracted from all gingival biopsies. Real-time PCR was performed to evaluate relative quantities of TLR-2 and TLR-4 mRNA. Statistical analyses were done using the Paired Wilcoxon test [2 related sample tests]. The relative expression levels of both TLR-2 and TLR-4 were significantly higher at diseased sites [2.41 +/- 2.06 and 1.25 +/- 1.16] than at healthy sites [0.91 +/- 1.04 and 0.41+0.60] [P<0.01]. Periodontal disease can significantly increase TLR-2 and TLR-4 gene expression in gingival tissues

Expression of IL-17 and COX2 gene in peripheral blood leukocytes of vitiligo patients

Vitiligo is a pigmentation disorder in which inflammatory mediators such as cytokines have a pivotal role in disease's pathogenesis. Interleukin 17 [IL-17A] is a proinflammatory cytokine which is involved in the induction of several proinflamatory mediators such as cyclooxygenase 2 [COX2]. The aim of this study was to investigate the gene expression of IL-17 and COX2 in peripheral blood leukocytes of vitiligo's patients. Peripheral blood leukocytes from 15 patients with vitiligo and 15 healthy controls were separated using a gradient density centrifugation method. After total RNA isolation and cDNA synthesis, IL-17 and COX2 gene expression were quantified by real-time polymerase chain reaction [PCR]. There were no significant differences in IL-17 and COX2 gene expression in lymphocytes of patients with vitiligo compared with control group [p<0.05]. However there was an increased IL-17 and COX2 gene expression in neutrophils of patients compared to controls, but it did not reach statistical significance [p=0.05]. We could not find any differences in IL-17 and Cox2 gene expression between clinical diseases subtypes, sex and age. There was a significant correlation between IL-17 and COX2 genes expression in the neutrophils of patients [p=0.00, r=0.80]. Our results showed an increased expression in IL-17 and Cox-2 genes in neurophils of patients with vitiligo. This suggested that these two factors are involved in the inflammatory process. Further studies with a larger sample size might help to establish the role of these factors in the pathogenesis of diseases

functional polymorphism of the granulocyte macrophage colony stimulating factor is not associated with the outcome of HTLV-I infection

Genetic background has known to be associated with the outcome of human T cell lymphotropic virus [HTLV] type I infection. In The present study we investigate the association between GM-CSF gene polymorphisms with the outcome of HTLV-I infection. We analyzed 3 single-nucleotide polymorphisms in the promter region of granulocyte macrophage colony stimulating factor [GM-CSF] at positions -677A/C, -1440A/G and -1916T/C in 68 patients with HTLV- I-associated myelopathy/tropical spastic paraparesis [HAM/TSP] and 77 HTLV-I-seropositive asymptomatic carriers and 175 healthy controls from an area in Iran, Mashhad, where HTLV-I is endemic. No significant differences were observed in the distribution of GM-CSF polymorphisms between HAM/TSP patients, HTLV-I carriers and healthy controls [P> 0.05]. The -611A/C polymorphism fall within the transcriptional enhancer factor-2 [TEF-2] binding site, so an electrophoretic mobility shift assay [EMSA] was performed to determine the effects of polymorphisms on protein binding to the GM-CSF promoter. The result showed a significantly higher binding efficiency of nuclear protein to the A allele compared with the C allele. Our study suggests that polymorphisms in the GM-CSF promoter is not associated with the outcome of HTLV-I infection, however, GM-CSF polymorphism at position -677 could indeed influence gene expression