2014
DOI: 10.1111/ocr.12033
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The effect of IL‐17 on the production of proinflammatory cytokines and matrix metalloproteinase‐1 by human periodontal ligament fibroblasts

Abstract: IL-17 upregulated the production of IL-6 and MMP-1 sequentially in HPDLF. IL-6/sIL-6R may enhance the effects of IL-1β on MMP-1 production. The present results suggest that IL-17 induces MMP-1 production not only directly, but also indirectly by promoting IL-6 production, thus resulting in the degradation of collagens in the PDL.

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Cited by 19 publications
(10 citation statements)
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“…IL-17 has multiple physiological functions. It activates macrophages to express TNF-α and IL-1β [26] and fibroblasts to produce IL-6, IL-8, and matrix metalloproteinases [27]. These cytokines are important for inflammatory process and tissue remodeling.…”
Section: Th17 Cells In Pathogenesis Of Psoriasismentioning
confidence: 99%
“…IL-17 has multiple physiological functions. It activates macrophages to express TNF-α and IL-1β [26] and fibroblasts to produce IL-6, IL-8, and matrix metalloproteinases [27]. These cytokines are important for inflammatory process and tissue remodeling.…”
Section: Th17 Cells In Pathogenesis Of Psoriasismentioning
confidence: 99%
“…IL-6 stimulus (0.1-1.0 ng mL À1 ) induced a mild dose-dependent mRNA expression and protein secretion of CRP in HPLF cultures, especially at 24 h, which was strongly enhanced by sIL-6R (1 and 5 ng mL À1 ), whereas the addition of anti-IL-6R blocking antibody abrogated these effects. The stimulatory conditions involved concentrations similar to physiologic ones (Radics et al 2003, compared to previous studies where 10-100 ng mL À1 of IL-6 and IL-6R was used (Hosokawa et al 2014, Shibata et al 2014.…”
Section: Discussionmentioning
confidence: 99%
“…The IL-17 is also associated with the upregulation of transforming growth factor beta (TGF- β ) signaling pathways [ 84 ], another potent promoter of atrial fibrosis and consequent AF [ 85 87 ]. In addition, IL-17 stimulates the production of more proinflammatory cytokines such as tumor necrosis factor- (TNF-) α and IL-6 [ 88 , 89 ] and regulates tissue infiltration by neutrophils and myocyte apoptosis, which can start and engage various other pathophysiological pathways including oxidative stress and hypercoagulability [ 90 92 ]. IL-17 induces the production of IL-6, a potent inductor of IL-17 synthesis, occurring in this way, a refeeding on the axis [ 73 , 74 ].…”
Section: Underlying Mechanisms Pathways and Relationship Betweenmentioning
confidence: 99%