AI Article Synopsis
- IL-17 is found in periodontal inflammation, indicating it may contribute to the inflammatory response.
- When tested on human gingival fibroblasts (HGFs), IL-17 increased IL-8 and minimally affected intercellular adhesion molecule (ICAM)-1, but did not influence HLA-DR or the immune-suppressive enzyme IDO.
- In contrast, IFN-gamma increased HLA-DR, ICAM-1, and IDO, but not IL-8; when both were combined, there was a significant enhancement in the expression of these molecules, suggesting their combined effect is crucial in immune modulation during periodontal disease.
Article Abstract
Interleukin (IL)-17 is present in inflammatory periodontal lesions, thus suggesting a role in mediating inflammation. We tested the hypothesis that IL-17, especially when combined with interferon (IFN)-gamma, may modulate the responses of human gingival fibroblasts (HGFs). IL-17 induced IL-8 and minimal intercellular adhesion molecule (ICAM)-1 expression. It had no effect on expression of HLA-DR, CD40, or the immune-suppressive enzyme indoleamine 2,3-dioxygenase (IDO). The effects of IL-17 on HGFs were compared with those of IFN-gamma. Unlike IL-17, IFN-gamma augmented the expression of HLA-DR, ICAM-1, and IDO, but not IL-8. Thus, IL-17 and IFN-gamma induce different HGF responses when administered separately. Interestingly, when IL-17 and IFN-gamma were combined, marked enhancement of ICAM-1, IL-8, and IDO expression by HGFs was observed. These findings suggest that IL-17, especially when combined with IFN-gamma, could play an important role in immune modulation through stimulation of HGFs in periodontal disease.
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| http://dx.doi.org/10.1177/154405910808700314 | DOI Listing |
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