INTERLEUKIN 1β-Secreting CELLS IN INFLAMED GINGIVAL TISSUE OF ADULT PERIODONTITIS PATIENTS

Yi-June, Lo; Liu, Cheing-Meei; Wong, Man-Ying; Hou, Linlin; Wei-Kuei, Chang

doi:10.1006/cyto.1999.0448

Cited by 32 publications

(7 citation statements)

References 34 publications

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“…[29] The staining of feline PDL cells for IL-1β showed the presence of bound signal complexes in the plasma membrane, which was expected, as it is known that receptors for IL-1β are present on fibroblasts. [30]…”

Section: Inflammatory Mediators In the Periodontal Ligamentmentioning

confidence: 81%

Biological response at the cellular level within the periodontal ligament on application of orthodontic force - An update

Meeran¹

2012

J Orthodont Sci

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Orthodontic force elicits a biological response in the tissues surrounding the teeth, resulting in remodeling of the periodontal ligament and the alveolar bone. The force-induced tissue strain result in reorganization of both cellular and extracellular matrix, besides producing changes in the local vascularity. This in turn leads to the synthesis and release of various neurotransmitters, arachidonic acid, growth factors, metabolites, cytokines, colony-stimulating factors, and enzymes like cathepsin K, matrix metalloproteinases, and aspartate aminotransferase. Despite the availability of many studies in the orthodontic and related scientific literature, a concise integration of all data is still lacking. Such a consolidation of the rapidly accumulating scientific information should help in understanding the biological processes that underlie the phenomenon of tooth movement in response to mechanical loading. Therefore, the aim of this review was to describe the biological processes taking place at the molecular level on application of orthodontic force and to provide an update of the current literature.

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Section: Inflammatory Mediators In the Periodontal Ligamentmentioning

confidence: 81%

Biological response at the cellular level within the periodontal ligament on application of orthodontic force - An update

Meeran¹

2012

J Orthodont Sci

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“…The main cause of periodontitis, bacterial plaque, triggers production of key cytokines, such as IL-1β and TNF-α, from macrophages. IL-1β, which has a wide range of biological activities, is known to have a strong association with the Gingival Index and pocket depth, and levels of IL-1β were significantly lower in healthy gingival tissue than in inflamed tissue in periodontitis patients [20]. TNF-α causes tissue destruction and an erosive reaction in periodontitis, and increased TNF-α levels are known to promote cartilage collagen degradation and bone resorption [21].…”

Section: Discussionmentioning

confidence: 99%

Antiperiodontitis Effects of Magnolia biondii Extract on Ligature-Induced Periodontitis in Rats

Lee

Choi

et al. 2019

Nutrients

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Over the past decades, periodontitis has become a rising health problem and caused various diseases. In the many studies shows that some extracts and compound to the prevention and treatment of periodontitis. This study focuses on the effects of inhibition of gingival damage and alveolar bone loss. The aim of this study was to evaluate the protective effects of Magnolia biondii extract (MBE) against ligature-induced periodontitis in rats. A ligature was placed around the molar teeth for 8 weeks, and MBE was administered for 8 weeks. Gingival tissue damage and alveolar bone loss were measured by microcomputed tomography (CT) analysis and histopathological examination. Serum Interluekin-1 β (IL-1β), tumor necrosis factor-α (TNF-α), cyclooxygenases-2 (COX-2), and receptor activator of nuclear factor–κB ligand (RANKL) levels were investigated using commercial kits to confirm the antiperiodontitis effects of MBE. We confirmed that ligature-induced periodontitis resulted in gingival tissue damage and alveolar bone loss. However, treatment for 8 weeks with MBE protected from periodontal tissue damage and downregulated serum inflammatory cytokine factors and RANKL levels. These results suggest that MBE exerts antiperiodontitis effects by inhibiting gingival tissue destruction and alveolar bone loss through regulation of anti-inflammatory cytokines in periodontitis-induced rats.

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“…Moreover, we found that MSCs express the CXCR3 chemokine receptor and can be upregulated by adding IL-1β. IL-1β is a pro-inflammatory cytokine and has been associated with inflammation [ 35 ] and tissue injury [ 36 ]. We then hypothesized that IL-1β-induced expression of CXCL9 in ECs and that IL-1β-induced CXCR3 expression on membrane of MSCs are related to MSC migration toward injured and inflamed tissue via the bloodstream.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-1β induces CXCR3-mediated chemotaxis to promote umbilical cord mesenchymal stem cell transendothelial migration

Guo¹,

Chiu²,

Chen

et al. 2018

Stem Cell Res Ther

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BackgroundMesenchymal stem cells (MSCs) are known to home to injured and inflamed regions via the bloodstream to assist in tissue regeneration in response to signals of cellular damage. However, the factors and mechanisms that affect their transendothelial migration are still unclear. In this study, the mechanisms involved in interleukin-1β (IL-1β) enhancing the transendothelial migration of MSCs were investigated.MethodsImmunofluorescence staining and Western blotting were used to observe IL-1β-induced CXC chemokine receptor 3 (CXCR3) expression on MSCs. Quantitative real-time PCR and ELISA were used to demonstrate IL-1β upregulated both chemokine (C-X-C motif) ligand 9 (CXCL9) mRNA and CXCL9 ligand secretion in human umbilical vein endothelial cells (HUVECs). Monolayer co-cultivation, agarose drop chemotaxis, and transwell assay were conducted to investigate the chemotaxis invasion and transendothelial migration ability of IL-1β-induced MSCs in response to CXCL9.ResultsIn this study, our immunofluorescence staining showed that IL-1β induces CXCR3 expression on MSCs. This result was confirmed by Western blotting. Following pretreatment with protein synthesis inhibitor cycloheximide, we found that IL-1β induced CXCR3 on the surface of MSCs via protein synthesis pathway. Quantitative real-time PCR and ELISA validated that IL-1β upregulated both CXCL9 mRNA and CXCL9 ligand secretion in HUVECs. In response to CXCL9, chemotaxis invasion and transendothelial migration ability were increased in IL-1β-stimulated MSCs. In addition, we pretreated MSCs with CXCR3 antagonist AMG-487 and p38 MAPK inhibitor SB203580 to confirm CXCR3-CXCL9 interaction and the role of CXCR3 in IL-1β-induced chemotaxis invasion and transendothelial migration.ConclusionWe found that IL-1β induces the expression of CXCR3 through p38 MAPK signaling and that IL-1β also enhances CXCL9 ligand secretion in HUVECs. These results indicated that IL-1β promotes the transendothelial migration of MSCs through CXCR3-CXCL9 axis. The implication of the finding could enhance the efficacy of MSCs homing to target sites.Electronic supplementary materialThe online version of this article (10.1186/s13287-018-1032-9) contains supplementary material, which is available to authorized users.

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INTERLEUKIN 1β-Secreting CELLS IN INFLAMED GINGIVAL TISSUE OF ADULT PERIODONTITIS PATIENTS

Cited by 32 publications

References 34 publications

Biological response at the cellular level within the periodontal ligament on application of orthodontic force - An update

Biological response at the cellular level within the periodontal ligament on application of orthodontic force - An update

Antiperiodontitis Effects of Magnolia biondii Extract on Ligature-Induced Periodontitis in Rats

Interleukin-1β induces CXCR3-mediated chemotaxis to promote umbilical cord mesenchymal stem cell transendothelial migration

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