Abstract
BackgroundThe production of chemokines by tissue resident cells during inflammation is considered one of the main mechanisms involved in the formation of inflammatory infiltrates. Fibroblasts are the main resident cell type in gingival and periodontal ligament tissues, and their ability to produce chemokine stromal cell-derived factor 1 alpha (SDF-1α) and its receptor CXCR4 under stimulation by gram negative bacteria, Porphyromonas gingivalis, commonly found in periodontal infections was investigated.MethodsWestern blots were used to assess SDF-1α and CXCR4 protein expression levels in human gingival fibroblast cells (HGF-1) induced by Lipopolysaccharide (LPS) from P. gingivalis in the presence or absence of LY294002, a highly selective inhibitor of PI-3K/Akt. RT-PCR and quantitative Real-time PCR was performed using gingival mRNAs from periodontitis patients. Immunohistochemistry was performed to analyze the expression and subcellular localization of SDF-1α and CXCR4, together with NF-kβ phosphorylation, in specimens from patients with periodontitis and in an experimental rat periodontitis model.ResultsWe found that P. gingivalis LPS up-regulated SDF-1α and CXCR4 protein levels and elevated phosphorylation of the SDF-1α-responsive NF-kβ and Akt at 24 h in HGF-1 cells. SDF-1α and CXCR4 mRNA and protein expression levels were high in all patients with periodontitis. In the P. gingivalis-induced rat experimental periodontitis model, SDF-1α and CXCR4 immunoreactivity was higher in gingival and periodontal ligament tissues compared to the control.ConclusionOur data showed that PI-3K/Akt is an upstream participant in the P. gingivalis LPS-mediated induction of SDF-1α. Taken together, these results suggest that the chemokine SDF-1α and its receptor CXCR4 contribute to P. gingivalis-induced periodontal inflammation.
Highlights
The production of chemokines by tissue resident cells during inflammation is considered one of the main mechanisms involved in the formation of inflammatory infiltrates
Effects of P. gingivalis LPS on the expression of stromal cell-derived factor 1 alpha (SDF-1α) and CXCR4 in human gingival fibroblasts (HGFs)-1 cells To understand whether inflammatory gingival activation alters the expression levels of SDF-1α and/or CXCR4, cultures of HGF-1 cells were exposed to P. gingivalis LPS at different concentrations, and SDF-1α and CXCR4 protein expression levels were evaluated by western blotting
Involvement of PI3-K/Akt in P. gingivalis LPS-induced expression of SDF-1α To determine whether the PI-3K/Akt cascade plays an important role in the LPS-induced expression of SDF-1α in HGF-1 cells, pre-treatment of HGF-1 cells with a pharmacological inhibitor of PI-3K, LY294002, significantly attenuated the P. gingivalis LPS-stimulated expression of SDF-1α, suggesting the involvement of PI-3K/Akt in that increased expression (Fig. 1b)
Summary
The production of chemokines by tissue resident cells during inflammation is considered one of the main mechanisms involved in the formation of inflammatory infiltrates. Fibroblasts are the main resident cell type in gingival and periodontal ligament tissues, and their ability to produce chemokine stromal cell-derived factor 1 alpha (SDF-1α) and its receptor CXCR4 under stimulation by gram negative bacteria, Porphyromonas gingivalis, commonly found in periodontal infections was investigated. The production of chemokines by those cells may vary significantly when comparing fibroblasts from different tissues [14,15,16], suggesting their important role in inflammatory infiltrate formation and cellular traffic during tissue repair. The chemokine CXCL12, known as stromal cellderived factor 1 alpha (SDF-1α), is constitutively expressed by human gingival fibroblasts (HGFs) and by human periodontal ligament (PDL) fibroblasts (HPDLFs). The involvement of SDF-1α in the progression of periodontal inflammation and its potential interactions with signaling cascades are not yet known
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