Gingival crevicular fluid infiltrating CD14+ monocytes promote inflammation in periodontitis

Saudi J Biol Sci. 2021 May;28(5):3069-3075. doi: 10.1016/j.sjbs.2021.02.049. Epub 2021 Feb 21.

Abstract

Periodontitis is a condition that occurs because of inflammation-mediated tissue degeneration. Many studies have been conducted to identify inflammatory molecules in periodontitis, but the well-defined role of cells from the immune system in the progression of periodontitis as well as in gingival tissue degeneration has not been appropriately established. The objective of the present study was to characterize the monocytes isolated from the gingival crevicular fluid (GCF) in patients with periodontitis. GCF was obtained from periodontitis patients and healthy controls. Cytokine levels of CCL2 were evaluated by ELISA in GCF samples. CD14+ monocytes were separated using magnetic sorting from GCF. RT-qPCR was performed to assess the gene expression. Cytometric bead array analysis was performed to analyze the levels of cytokines and chemokines in the secretome of cells. CD14+ monocytes from GCF secreted higher levels of CCL2 and showed elevated expression of genes responsible for monocyte migration. Additionally, upon lipopolysaccharide stimulation, these monocytes secreted higher levels of inflammatory cytokines and chemokines. This investigation aids in understanding the inflammatory microenvironment of periodontitis by characterizing GCF in terms of infiltrated CD14+ monocytes, cytokines, and molecules secreted by these monocytes, which are specific for cellular differentiation.

Keywords: CCL2, C-C motif chemokine ligand 2; CCL3, C-C motif chemokine ligand 3; CCL5, C-C motif chemokine ligand 5; CCR1, C-C chemokine receptor type 1; CCR2, C-C chemokine receptor type 2; CCR5, C-C chemokine receptor type 5; CD11b (ITGAM), Integrin alpha M; CD14+ monocytes; CXCR5/BLR1, C-X-C chemokine receptor type 5; Gingival crevicular fluid; IL-1β, Interleukin 1 beta; IL-6, Interleukin 6; IL-8, Interleukin 8; Inflammatory cytokines; Periodontitis; STAT1, Signal transducer and activator of transcription 1; STAT2, Signal transducer and activator of transcription 2; STAT6, Signal transducer and activator of transcription 6; TNF-α, Tumor necrosis factor-alpha.