تحريك پذيري سلولهاي منوسيت خون محيطي افراد مبتلا به پريودنتيت مهاجم از طريق مقايسه ميزان اينترلوكين 6 ترشح شده ، قبل و پس از تحريك باليپوپلي ساكاريد باكتري اشريشياكلي

Peripheral blood monocytes responsiveness in aggressive periodontitis patients by comparison of Interleukin-6 production before and after stimulation by E.coli lipopolysacharide

Objective Results of other studies suggests that hyper-responsiveness of monocytes to the products of dental plaque especially the endotoxin of Gram negative bacteria and secretion of high levels of pro-inflammatory cytokines may have a role in the pathogenesis of AP. To investigate this possibility, we evaluated the IL-6 production by cultured peripheral blood monocytes before and after stimulation by E.coli lipopolysacharide (LPS) in AP patients and healthy controls. Materials and Methods Fifteen patients with AP were compared to 15 periodontal healthy controls in a case control study. Mononuclear layer was obtained from peripheral blood samples and monocytes were isolated and cultured. The reaction of monocytes was studied by IL-6 production before and 6 hours after stimulation by 0.1 µg/ml E.coli. LPS. The IL-6 concentration in the culture supematant was measured with ELISA(Enzyme linked Immunosorbent Assay). 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 (P = 0.5). The IL-6 production after LPS stimulation in the patients was higher than controls, and the difference approached the significance threshold (P = 0.07). However, the increase in the IL-6 production as a result of LPS stimulation was significantly higher in patients compared to controls (P = 0.029). Conclusion Our results suggest that increase in monocyte responsiveness may play a potential role in the pathogenesis of AP. Elevation in cytokines elicited at the site of infection in response to a minimal bacterial challenge can exert significant effects locally and systemically. An over-aggressive immune response can provide the basis of explanation for the observed severe tissue damage and bone loss in periodontium, familial nature of aggressive periodontitis and other immunological findings associated with the pathogenesis of this disease. Future investigations through longitudinal monitoring of monocyte responsiveness over time and following successful treatment are required to elucidate the role of this phenomenon in the pathogenesis of periodontitis.