Overexpression and Potential Regulatory Role of IL-17F in Pathogenesis of Chronic Periodontitis.
The objective of this study was to investigate the expression level, clinical significance, and possible regulating role of IL-17F in patients of chronic periodontitis. Periodontal local tissues were obtained from chronic periodontitis (CP) and healthy controls (HC) for real-time PCR (RT-PCR) detection with IL-17F and IL-17A messenger RNA (mRNA). Primary human gingival fibroblasts (HGF) were derived from patients receiving crown-lengthening procedures. Efficiency of small interfering RNA (siRNA) of IL-17R to HGF cells were assessed by Western blot and RT-PCR. Recombinant IL-17F and IL-17A were used to stimulate the HGF cells compared with the control group. Aspects of the nuclear factor-kappa B (NF-κB) and extracellular signal-regulated kinase (ERK) signaling pathways were examined by Western blot. Production of pro-inflammatory cytokines induced by IL-17F and IL-17A was detected by RT-PCR. Statistical analysis was analyzed by SPSS software. It showed significantly elevated levels of IL-17F and IL-17A mRNA in CP gingival tissues compared with HC group (P<0.01). Further analysis showed a significant correlation between IL-17F and IL-17A mRNA in CP group (P<0.05), and both cytokines also correlated with the probing depth (P<0.05). Recombinant IL-17F can induce NF-κB phosphor-p65 and ERK phosphorylation of HGF cells similar to that of IL-17A. Interestingly, we found that both IL-17F and IL-17A could promote the important inflammatory cytokines IL-6, CXCL8, and CCL20 production compared with IL-17R siRNA group (P<0.05). This study indicates that IL-17F may be involved in pathogenesis of periodontitis like IL-17A. The role of IL-17F in disease pathogenesis needs to be further investigated.
Department of Periodontics, School of Stomatology, Capital Medical University, Beijing, China.
Zhenhua
Z
Luo
Hui
H
Wang
Jiajun
J
Chen
Jian
J
Kang
Zheng
Z
Sun
Yafei
Y
Wu
D000328:Adult; D002478:Cells, Cultured; D054418:Chemokine CCL20 / Q000096:biosynthesis; D055113:Chronic Periodontitis / Q000276:immunology / Q000473:pathology*; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D005260:Female; D005347:Fibroblasts; D005881:Gingiva / Q000166:cytology / Q000473:pathology*; D006801:Humans; D020381:Interleukin-17 / Q000235:genetics / Q000378:metabolism*; D015850:Interleukin-6 / Q000096:biosynthesis; D016209:Interleukin-8 / Q000096:biosynthesis; D008297:Male; D010766:Phosphorylation; D034622:RNA Interference; D012333:RNA, Messenger / Q000235:genetics; D034741:RNA, Small Interfering; D053722:Receptors, Interleukin-17 / Q000235:genetics; D011994:Recombinant Proteins / Q000494:pharmacology; D015398:Signal Transduction; D051996:Transcription Factor RelA / Q000378:metabolism
C108355:CCL20 protein, human; C508606:CXCL8 protein, human; D054418:Chemokine CCL20; C508717:IL17A protein, human; C440021:IL17F protein, human; C109985:IL17RA protein, human; C508600:IL6 protein, human; D020381:Interleukin-17; D015850:Interleukin-6; D016209:Interleukin-8; C498143:RELA protein, human; D012333:RNA, Messenger; D034741:RNA, Small Interfering; D053722:Receptors, Interleukin-17; D011994:Recombinant Proteins; D051996:Transcription Factor RelA; D048049:Extracellular Signal-Regulated MAP Kinases