Title of article :
Suppression of interleukin-10 release from human periodontal ligament cells by interleukin-1β in vitro
Author/Authors :
Deschner، نويسنده , , J and Arnold، نويسنده , , B and Kage، نويسنده , , A and Zimmermann، نويسنده , , B and Kanitz، نويسنده , , V and Bernimoulin، نويسنده , , J.-P، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2000
Pages :
5
From page :
179
To page :
183
Abstract :
Periodontitis is characterized by an inflammatory process induced by periodontopathogenic bacteria in the subgingival plaque. Periodontal inflammation can be enhanced by both an increase of inflammatory stimulators, e.g. interleukin (IL)-6, and a decrease of inflammatory inhibitors, e.g. IL-10. The amount of IL-1β is known to be increased in gingival tissues and in the gingival crevicular fluid from inflamed sites compared to healthy sites. This in vitro study sought to clarify whether IL-1β (1 ng/ml) has a regulatory effect on the release of these two cytokines from human periodontal ligament (PDL) cells. PDL cells derived from healthy premolars were grown in the presence and absence (control) of IL-1β. The concentration of IL-6 and IL-10 in the supernatants was assessed by enzyme-linked immunosorbent assay after 48 h of culture. PDL cells incubated with IL-1β released significantly (p<0.05) higher amounts of IL-6 and significantly (p<0.01) smaller amounts of IL-10 compared to control. These results give further support to the observation that IL-1β can increase the IL-6 secretion from PDL cells. Moreover, they provide original evidence that PDL cells secrete IL-10, which can be suppressed by IL-1β. It is concluded that PDL cells can function as accessory immunoinflammatory cells amplifying the inflammatory process in periodontitis and, thereby, contributing to periodontal breakdown.
Keywords :
Interleukin-10 , Periodontitis , Interleukin-1? , cytokine , Periodontal ligament , Cell culture
Journal title :
Archives of Oral Biology
Serial Year :
2000
Journal title :
Archives of Oral Biology
Record number :
1801561
Link To Document :
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