Tuesday, January 21, 2020

Expression of colony‐stimulating factor 1 and interleukin‐34 in gingival tissue and gingival fibroblasts from periodontitis patients and controls

Abstract

Background

Colony‐stimulating factor 1 (CSF‐1) and interleukin (IL)‐34 are important for the functions of myeloid lineage cells and are involved in several chronic inflammatory conditions associated with tissue degeneration. The aim of this study is to evaluate the expression of CSF‐1 and IL‐34 in gingival tissue and gingival fibroblasts (GF) from patients with periodontitis and controls.

Methods

Gingival biopsies were obtained from 19 periodontitis patients and 15 controls. Expression of CSF‐1 and IL‐34 in gingival tissue was assessed by western blot and localization by immunohistochemistry. Expression of CSF1 and IL34 mRNA in GF was analyzed by real‐time polymerase chain reaction and protein expression visualized by immunofluorescence stainings. CSF‐1 and IL‐34 secretion from GF was evaluated in response to tumor necrosis factor‐alpha (TNF‐α), IL‐1β, Escherichia coli lipopolysaccharide (Ec‐LPS) and Porphyromonas gingivalis lipopolysaccharide (Pg‐LPS) stimulation, using enzyme‐linked immunosorbent assays.

Results

CSF‐1 was increased in gingival tissue from periodontitis patients compared with controls (P < 0.05) whereas IL‐34 expression was similar. In GF from a non‐periodontitis donor, stimulation with either TNF‐α, IL‐1β, Ec‐LPS, or Pg‐LPS, increased the secretion of CSF‐1 (P < 0.05) and Ec‐LPS stimulation increased IL‐34 (P < 0.05). CSF‐1 and IL‐34 were expressed and secreted constitutively from GF, with comparable levels in GF from periodontitis patients and controls. Inflammatory stimuli increased the secretion of CSF‐1 and IL‐34 with comparable levels measured from GF from periodontitis patients and controls (P < 0.05).

Conclusion

The expression of CSF‐1 and IL‐34 in gingival tissue and fibroblasts suggests involvement in myeloid cell functions during periodontal inflammation.



from
https://onlinelibrary.wiley.com/doi/abs/10.1002/JPER.19-0296?af=R

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