外周血单个核细胞
牙周炎
肿瘤坏死因子α
免疫学
脂多糖
医学
白细胞介素
炎症
化学
细胞因子
内科学
生物化学
体外
作者
Anders Gustafsson,H. Ito,B. Åsman,Kurt Bergström
标识
DOI:10.1111/j.1600-051x.2005.00883.x
摘要
Abstract Objectives: Stimulated mono‐ and polymorphonuclear cells from patients with periodontitis have shown increased release of interleukin‐1 β (IL‐1 β ) and oxygen radicals, respectively. The aim was to study whether this hyper‐reactivity could be found both in mono‐ and polymorphonuclear cells from the same patient, and whether there was a relation to the gene coding for IL‐1 β (IL‐1 β +3953 ). Material and Methods: Peripheral mononuclear cells from 14 non‐smoking and well‐treated patients and pair‐matched controls were incubated with opsonized Staphylococcus aureus and lipopolysaccharide (LPS). Released IL‐1 β and tumour necrosis factor (TNF)‐ α were determined with ELISA. Generation of oxygen radicals from the Fc γ ‐receptor‐stimulated neutrophils was measured with chemiluminescence and the polymorphism at IL‐1 β +3953 was measured with polymerase chainreaction. Results: The mononuclear cells from the patients released more IL‐1 β after incubation with LPS ( p <0.001) and with bacteria ( p <0.05). The release of TNF‐ α tended to be higher in the patient group. The peripheral neutrophils from the patients generated more oxygen radicals ( p <0.06). We found no differences between the study groups regarding the IL‐1 β +3953 polymorphism. Conclusion: The similarity in systemic inflammation between patients and controls suggests that the increased release/generation of IL‐1 β and oxygen radicals from peripheral leukocytes in periodontitis patients is of a constitutional nature and of pathogenic relevance.
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