These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Interleukin-6 production by cultured peripheral blood monocytes before and after stimulation by E. coli lipopolysaccharide in Iranian patients with aggressive periodontitis. Author: Bajestan MN, Radvar M, Afshari JT, Naseh MR, Arab HR. Journal: Med Sci Monit; 2006 Sep; 12(9):CR393-6. PubMed ID: 16940934. Abstract: 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.[Abstract] [Full Text] [Related] [New Search]