LPS induces GROα chemokine production via NF-κB in oral fibroblasts

Jönsson, Daniel; Amisten, Stefan; Bratthall, Gunilla; Holm, Anna; Nilsson, Bengt‐Olof

doi:10.1007/s00011-009-0049-z

Cited by 22 publications

(14 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Taken together, estrogen exerts both anti‐inflammatory and pro‐inflammatory effects via these mechanisms. We have previously shown that the chemokine GROα, which is another important chemoattractant for neutrophils, is also, like CCL2, not regulated by estrogen (34). In this study we showed that both CCL3 and CCL5 are regulated by estrogen, while CCL2 is not.…”

Section: Discussionmentioning

confidence: 99%

Differential regulation of chemokine expression by estrogen in human periodontal ligament cells

Nebel

Jönsson

Norderyd

et al. 2010

Journal of Periodontal Research

Self Cite

View full text Add to dashboard Cite

Nebel D, Jönsson D, Norderyd O, Bratthall G, Nilsson B‐O. Differential regulation of chemokine expression by estrogen in human periodontal ligament cells. J Periodont Res 2010; 45: 796–802. © 2010 John Wiley & Sons A/S Background and Objective: Estrogen modulates inflammatory responses, but the mechanisms involved have not yet been identified. Periodontal ligament (PDL) cells produce chemokines (a group of chemoattractant molecules that recruit leukocytes) and it has been suggested that estrogen modulates periodontal inflammation by regulating the expression of chemokines by PDL cells. Therefore, the objectives of this study were to investigate the regulation of chemokine ligand 2 [CCL2/monocyte chemoattractant protein 1 (MCP‐1)], chemokine ligand 3 [CCL3/macrophage inflammatory protein‐1α (MIP‐1α)] and chemokine ligand 5 (CCL5/RANTES) by estrogen in human PDL cells. Material and Methods: PDL cells were obtained from the PDL of premolars, extracted for orthodontic reasons, from two boys and two girls (16 and 17 years of age). PDL cell CCL2, CCL3 and CCL5 mRNA transcripts were determined by quantitative real‐time PCR. The concentrations of CCL2, CCL3 and CCL5 proteins were determined by ELISAs. Results: Treatment with 0.5 μg/mL of lipopolysaccharide (LPS, from Escherichia coli) + 100 nm 17β‐estradiol (E2) for 24 h reduced the expression of CCL3 mRNA by about 40% compared to PDL cells treated with LPS alone. Attenuation of CCL3 mRNA was not associated with a decrease in CCL3 protein within 48 h, suggesting a slow turnover of the CCL3 protein. Interindividual differences in the effects of E2 on CCL5 mRNA expression were observed. E2 (100 nm) increased the expression of CCL5 by 40–60% in PDL cells derived from two subjects but reduced the expression of CCL5 by about 30% in cells from another subject. CCL2 mRNA and CCL2 protein were highly expressed, but not regulated by E2. Similar data were observed in cells obtained from both boys and girls. Conclusion: Regulation, by estrogen, of chemokine expression in PDL cells shows a complex pattern involving the down‐regulation as well as the up‐regulation of chemokines, suggesting that estrogen exerts both anti‐inflammatory and proinflammatory effects through these mechanisms.

show abstract

Section: Discussionmentioning

confidence: 99%

Differential regulation of chemokine expression by estrogen in human periodontal ligament cells

Nebel

Jönsson

Norderyd

et al. 2010

Journal of Periodontal Research

Self Cite

View full text Add to dashboard Cite

show abstract

“…Lipopolysaccharide also induces cytokine production in human gingival fibroblasts (10,11), suggesting that periodontal ligament cells and gingival fibroblasts act together to promote proinflammatory actions. Cytokine and chemokine production by periodontal ligament cells is observed in response to stimulation with low, intermediate and high concentrations (1 ng/mL to 10 μg/mL) of LPS (12,13). Lipopolysaccharide‐induced periodontal ligament cell cytokine/chemokine expression is observed within hours but also after several days (3–21 d) of treatment, showing that both acute and long‐term stimulation with inflammation promoters activate cell‐signalling pathways leading to cytokine/chemokine production (12).…”

Section: Inflammation Promoters Stimulate Periodontal Ligament Cell Cmentioning

confidence: 99%

“…Human periodontal ligament cells accumulate radioactive ([ 3 H]‐labelled) dexamethasone, suggesting that periodontal ligament cells express the glucocorticoid receptor (18). Treatment with dexamethasone has been shown to reduce tumour necrosis factor‐α‐induced interleukin‐6 and interleukin‐8 production (19,20) and to reduce LPS‐induced chemokine ligand 1 (GROα) chemokine expression (13) in human periodontal ligament cells. Besides suppressing cytokine/chemokine production via inhibition of NF‐κB, dexamethasone drives the periodontal ligament cells towards an osteoblastic phenotype (21).…”

Section: Glucocorticoids and Human Periodontal Ligament Cellsmentioning

confidence: 99%

The human periodontal ligament cell: a fibroblast-like cell acting as an immune cell

Jönsson

Nebel

Bratthall

et al. 2010

Journal of Periodontal Research

Self Cite

141

123

View full text Add to dashboard Cite

show abstract

“…In human PDL cells, LPS-stimulation strongly enhances the production of both IL-6 and MCP-1 [12]. LPS enhances cytokine expression primarily via binding to the Toll-like receptors (TLR4 and TLR2), and this complex then activates signaling via the nuclear factor kappa light chain enhancer of activated B cells (NF-κB) pathway leading to transcription of cytokine genes [13, 14]. …”

Section: Introductionmentioning

confidence: 99%

Secretory leukocyte protease inhibitor regulates human periodontal ligament cell production of pro-inflammatory cytokines

et al. 2017

Self Cite

View full text Add to dashboard Cite

ObjectiveRegulation of immune-like cell properties of periodontal ligament (PDL) cells is not understood. We investigate the importance of secretory leukocyte protease inhibitor (SLPI) for production of pro-inflammatory cytokines in human PDL cells.Materials and methodsPDL cells were isolated from teeth extracted for orthodontic reasons. Cellular location of SLPI was investigated by immunocytochemistry. Cytokine transcript and protein expression were assessed by quantitative real-time RT-PCR and Western blotting. SLPI gene activity was knocked-down by siRNA. NF-κB signaling was assessed by measuring IκBα, and phosphorylated p65 and p105 protein expression.ResultsPDL cells showed cytoplasmic expression of SLPI. Cellular expression level of SLPI negatively correlated to LPS-induced stimulation of IL-6 and MCP-1. Both SLPI gene activity and protein were reduced by about 70% in PDL cells treated with SLPI siRNA compared to cells treated with non-coding construct. Treatment with SLPI siRNA was associated with up-regulation of both basal and LPS-stimulated IL-6, MCP-1 and TLRs mRNA expression. The up-regulation of MCP-1 transcript in SLPI siRNA-treated cells was confirmed on protein level. SLPI siRNA-treatment enhanced the phosphorylated NF-κB p105 protein expression.ConclusionsSLPI regulates PDL cell pro-inflammatory cytokine expression and modulates NF-κB signaling, suggesting that SLPI governs the immune cell-like properties of PDL cells.

show abstract

LPS induces GROα chemokine production via NF-κB in oral fibroblasts

Abstract: Oral fibroblasts respond to LPS stimulation by increasing GROalpha production via the transcription factor NF-kappaB, suggesting that this mechanism may be involved in development of periodontal inflammation.

Cited by 22 publications

References 29 publications

Differential regulation of chemokine expression by estrogen in human periodontal ligament cells

Differential regulation of chemokine expression by estrogen in human periodontal ligament cells

The human periodontal ligament cell: a fibroblast-like cell acting as an immune cell

Secretory leukocyte protease inhibitor regulates human periodontal ligament cell production of pro-inflammatory cytokines

Contact Info

Product

Resources

About