The effect of periodontal treatment on IL-6 production of peripheral blood monocytes in aggressive periodontitis and chronic periodontitis patients.

BACKGROUND: Several cytokines, including IL-6 have been implicated in the pathogenesis of periodontal disease. It is established that monocytes from periodontitis subjects show an increased production of IL-6 as compared to healthy subjects. However, little is known about the effect of periodontal treatment on IL-6 production by monocytes in subsets of periodontitis patients. OBJECTIVE: The aim of the present study was to evaluate the effect of surgical periodontal treatment on IL-6 production of peripheral blood monocytes (PBM) in aggressive periodontitis patients (AP) and chronic periodontitis patients (CP) before and after stimulation by E.coli LPS. METHODS: Fifteen AP patients, 15 CP patients and 15 periodontally healthy subjects (PH) took part in the study. PBM IL-6 pro-duction was measured, using ELISA, before and after stimulation of cultured PBM cells by 0.1 microg/ml LPS of E.coli. Following full-mouth non-surgical and surgical periodontal treatment of the AP and CP groups, the same measurements were repeated for these two groups. RESULTS: LPS-stimulated IL-6 production was significantly greater than non-stimulated IL-6 for all 3 groups. Before periodontal treatment, LPS-stimulated IL-6 pro-duction of the AP group was significantly greater than the other 2 groups. Periodontal treatment did not result in a significant decrease in unstimulated or LPS-stimulated IL-6 production by PBM cells in AP and CP patients. No correlation was detected between IL-6 levels and baseline clinical parameters or changes in clinical parameters. CONCLUSION: PBM cells in AP patients might be hyper-responsive in terms of IL-6 production. This hyper-responsiveness does not seem to return to that of healthy subjects even after a successful periodontal treatment. Moreover, the regulation of host inflammatory mechanisms upon LPS challenge might be different between AP and CP patients.

Interleukin-6 production by cultured peripheral blood monocytes before and after stimulation by E. coli lipopolysaccharide in Iranian patients with aggressive periodontitis.

BACKGROUND: It has been suggested that hyper-responsiveness of monocytes to the products of dental plaque, especially the endotoxin of Gram-negative bacteria and the secretion of high levels of pro-inflammatory cytokines, may have a role in the pathogenesis of aggressive periodontitis (AP). To investigate this possibility, IL-6 production by cultured peripheral blood monocytes before and after stimulation by E. coli lipopolysaccharide (LPS) in AP patients was evaluated. MATERIAL/METHODS: Fifteen patients with AP were compared with 15 periodontally healthy controls in a case control study. Monocytes were obtained from peripheral blood samples and cultured. The reaction of monocytes was studied by their IL-6 production using ELISA before and six hours after stimulation by 0.1 microg/ml E. col. LPS. The Wilcoxon and Mann-Whitney U tests were used to compare the groups. RESULTS: There was no significant difference in IL-6 production levels before LPS stimulation between patients and controls. Upon LPS stimulation, IL-6 levels increased in both the patient and control groups compared with their IL-6 levels before stimulation. IL-6 production after LPS stimulation in the patients was higher than controls, but this was not statistically significant. However, the increase in IL-6 production as a result of LPS stimulation was significantly higher in patients than in controls. CONCLUSIONS: Increased monocyte responsiveness may play a potential role in the pathogenesis of AP. However, whether this is an intrinsic characteristic of the monocyte/macrophage cells of AP patients or just a priming effect as a result of the periodontal disease remains to be investigated.

Association of AKT1 haplotype with the risk of schizophrenia in Iranian population.

AKT-glycogen synthase kinase 3beta (GSK3beta) signaling is a target of lithium and has been implicated in the pathogenesis of mood disorders and schizophrenia. AKT1 protein level is decreased in the peripheral lymphocytes and brains of schizophrenic patients. The SNP2/3/4 TCG haplotype of AKT1 was associated with schizophrenia in patients with Northern European origin. In the present study, we genotyped five single nucleotide polymorphisms (SNP1-5) of AKT1 gene according to the original study in Iranians comprising of 321 schizophrenic patients and 383 controls, all residing in Mashhad city, Northeastern Iran. Haplotype analysis showed that the frequency of a five-SNP haplotype (AGCAG) was significantly higher in schizophrenic patients (0.068) than that of controls (0.034) (P = 0.03 after Bonferroni correction, OR = 2.04, CI = 1.2-3.4). In stratified analysis by schizophrenia subtypes, the frequency of the same haplotype was significantly higher in disorganized subtype (n = 78, frequency of haplotype=0.081) when compared with normal controls (P = 0.04 after Bonferroni correction, OR = 2.59, CI = 1.3-5.2). Our findings did not confirm the association of AKT1 SNP2/3/4 TCG haplotype with the risk of schizophrenia as reported in the original study but showed the evidence of association with a different haplotype, AKT1 five-SNP AGCAG haplotype, with the risk of schizophrenia in Iranian population.