Background/purpose
Recurrent aphthous ulceration (RAU) has an incidence of approximately 20% in general population. However, its exact cause remains unknown. Increasing evidence suggests that immunologic mechanisms may play crucial roles in the etiology of this disease.
Materials and methods
The peripheral blood samples were obtained from 85 patients with RAU during acute phase and 87 healthy controls. The serum levels of IgG, IgA, IgM, C3 and C4 were measured by immunoturbidimetry. In addition, the serum IgE levels were measured by electro-chemiluminescence immunoassay. Furthermore, the percentages of B, T, CD4
+
T, CD8
+
T lymphocytes and natural killer (NK) cells in peripheral blood were determined by flow cytometry.
Results
Our findings showed that the serum IgG, IgA, IgE, C3 and C4 levels of RAU patients were significantly higher than those of healthy controls. The percentages of CD4
+
T cells and B cells in peripheral blood of RAU patients were significantly decreased, whereas the percentages of CD8
+
T cells and NK cells of RAU patients were remarkably increased. Our results indicated that the IgG level was elevated in 18 patients (21.2%) and that the IgE level was increased in 21 patients (24.7%). Our results also showed that the frequency of abnormal IgG or IgE levels were significantly correlated with that of abnormal CD8
+
T cell percentage in RAU patients.
Conclusion
The levels of both humoral and cellular immune components could be altered in RAU. The relationship between humoral and cellular immune may be potentially important immunologic aspects involved in the pathogenesis of RAU.
PurposeEvidence on the contribution of genes to the hereditary predisposition to pulmonary arterial hypertension (PAH) is limited.Materials and MethodsIn this study, we hypothesized that single nucleotide variants in vascular endothelial growth factor (VEGF) gene may alter gene function and expression and may be associated with PAH risk. Five putatively functional loci (rs699947C>A and rs833061T>C in the promoter, rs3025040C>T, rs10434G>A and rs3025053G>A in the 3'-UTR) in the VEGF gene were genotyped and analyzed in a retrospective study of 587 patients with PAH and 736 healthy subjects from southern China.ResultsWe found that the rs833061T>C polymorphism was significantly associated with PAH risk, while the other single nucleotide polymorphisms were not. Compared to carriers with TT genotype, those with rs833061C variant genotype (CT/CC) had an increased risk of PAH (odds ratio=1.47, 95% confidence interval=1.18–1.83, p=0.001). Functional assays indicated that CT/CC variant genotype had significantly higher mRNA levels of VEGF in peripheral blood mononuclear cells than TT genotype (p=0.021). Luciferase reporter assay indicated that having a C allele conferred a significantly higher transcription activity than that with a T allele.ConclusionOur findings suggest that the functional polymorphism rs833061T>C in VEGF gene promoter modulates VEGF expression and may be a valuable biomarker for predicting PAH susceptibility.
Cigarette smoking is an established risk factor for some oral diseases. As an essential fluid in the oral cavity, saliva is crucial to maintain oral health. Relative to active smoking, there are very few studies assessing the effect of passive smoking on salivary cytokines levels. In the present study, we established the rat models by the means of the intraoral cigarette smoking or whole body cigarette smoke exposure to simulate human active or passive smoking, respectively. The effects of active or passive smoking on salivary cytokines levels were assessed by using ProcartaPlex multiplex immunoassays. The results of the current study indicated that both active and passive smoking diminished the body weights of rats and increased the levels of some blood counts. Intriguingly, active smoking enhanced the salivary levels of IL-6 and IL-12 p70 and passive smoking elevated the salivary IL-6 level. Moreover, active smoking appeared to have a more prominent activation effect on the salivary IL-6 level. It was noted that active or passive smoking had no significant effect on the salivary IFNlevel. Active or passive smoking could have potential effects on the salivary levels of some pro-inflammatory cytokines.
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