Expression of fractalkine (CX3CL1) and its receptor, CX3CR1, in periodontal diseased tissue

Abstract

SummaryThe regulatory role of chemokines and chemokine receptors on specific leucocyte recruitment into periodontal diseased tissue is poorly characterized. We observed that leucocytes infiltrating inflamed gingival tissue expressed marked levels of CX3CR1. In periodontal diseased tissue, the expression of fractalkine and CX3CR1 mRNA was detected by reverse transcriptionpolymerase chain reaction (RT-PCR) and further, fractalkine was distributed mainly on endothelial cells, as shown by immunohistochemistry. Moreover, we can detect CX3CR1-expressing cells infiltrated in periodontal diseased tissue by immunohistochemical staining. Furthermore, fractalkine production by human umbilical vein endothelial cells (HUVEC) was up-regulated by pathogen-associated molecular patterns (PAMPs), including Porphyromonas gingivalis lipopolysaccharide (LPS). Thus, these findings suggested that CX3CR1 and the corresponding chemokine, fractalkine may have an important regulatory role on specific leucocyte migration into inflamed periodontal tissue.

Catechins inhibit CXCL10 production from oncostatin M-stimulated human gingival fibroblasts

“…Single-strand cDNA for a PCR template was synthesized from 48 ng of total RNA using the oligo(dT) [12][13][14][15][16][17][18] primer (Invitrogen, Carlsbad, CA, USA) and superscript3 reverse transcriptase (Invitrogen) under the conditions indicated by the manufacturer. Specific primers were designed from cDNA sequences for gp130, OSM receptor beta (OSMRβ) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH).…”

“…The disease initiation and progression result from the host response to plaque bacteria. Immunohistochemical studies have revealed dense inflammatory cell infiltration, including T and B cells and macrophages in periodontitis-affected regions [14][15][16][17][18][19]. Recently, several studies demonstrated that Th1 cells are involved in bone resorption in oral cavities.…”

CX3CL1 expression induced by Candida albicans in oral fibroblasts

“…Some investigators have reported that inflammatory cytokines and bacterial factors induced CX3CL1 in human vascular endothelial cells (HUVEC). Th1 cytokine, IFN‐γ enhanced CX3CL1 expression in HUVEC (Hatakeyama et al , 2004), while E. coli lipopolysaccharide and Porphyromonas gingivalis lipopolysaccharide significantly induced CX3CL1 production by HUVEC (Hosokawa et al , 2006). In the present study, CX3CL1 mRNA expression in both GT1 and RT7 cells was not induced by S. aureus, E. coli heat‐killed cells or TNF‐α (Fig.…”

Black tea polyphenol inhibits CXCL10 production in oncostatin M-stimulated human gingival fibroblasts

“…The disease initiation and progression result from host response to plaque bacteria. Immunohistochemical studies revealed dense inflammatory cells infiltration, including T and B cells and macrophages in the periodontitis region [20][21][22][23][24][25]. Several studies demonstrated that Th1 cells are involved in bone resorption in oral cavity inflammation.…”