Oral fibroblasts modulate the macrophage response to bacterial challenge

Abstract

Tissue damage in chronic periodontal disease is driven by the host response to a dysbiotic microbiota, and not by bacteria directly. Among chronic inflammatory diseases of the oral cavity, inflammation and tissue damage around dental implants (peri-implantitis) is emerging as a major clinical challenge, since it is more severe and less responsive to treatment compared to inflammation around natural teeth. We tested whether oral fibroblasts from the periodontal ligament (PDLF), which are present around natural teeth but not around dental implants, actively regulate inflammatory responses to bacterial stimulation. We show that human PDLF down-regulate TNF-α post-transcriptionally in macrophages stimulated with the oral pathogen Porphyromonas gingivalis. Cell contact and secretion of IL-6 and IL-10 contribute to the modulation of inflammatory cytokine production. Although fibroblasts decreased TNF-α secretion, they enhanced the ability of macrophages to phagocytose bacteria. Surprisingly, donor matched oral fibroblasts from gingival tissues, or fibroblasts from peri-implant inflamed tissues were at least as active as PDLF in regulating macrophage responses to bacteria. In addition, priming fibroblasts with inflammatory mediators enhanced PDLF regulatory activity. A further understanding of the spectrum of fibroblast activities in inflammatory lesions is important in order to design ways to control inflammatory tissue damage.

Surface characterization of titanium implant healing abutments before and after placement

“…However, the integrity of this soft tissue seal is also vulnerable to bacteria, especially immediately post‐surgery . A study by Zhao and colleagues and others presented the idea of a “race‐for‐the‐surface” between bacterial cells and mammalian gingival cells as a defining factor in the establishment of this soft tissue seal, and overall soft‐tissue health . Although this phenomenon has been primarily emphasized when considering soft‐tissue attachment implants, the race‐for‐the‐surface can occur on any component of the implant system that is simultaneously exposed to bacteria and cells .…”

“…33 A study by Zhao and colleagues and others presented the idea of a "race-for-the-surface" between bacterial cells and mammalian gingival cells as a defining factor in the establishment of this soft tissue seal, and overall soft-tissue health. 33,[37][38][39][40] Although this phenomenon has been primarily emphasized when considering soft-tissue attachment implants, the race-forthe-surface can occur on any component of the implant system that is simultaneously exposed to bacteria and cells. 39,41,42 Therefore, in order to understand the conditions in which this soft tissue health is compromised, components associated with early stage healing of gingiva need to be better investigated.…”

Initial periodontal treatment affects nucleotide-binding domain leucine-rich repeat-containing protein 3 inflammasome priming in peripheral blood mononuclear cells

“…The cDNA was treated with RNase H and purified using the QIAprep Spin Miniprep Kit (Qiagen). The primer sequences used were as follows: IL-1β forward, 5′-GCTGGAGGACTTT AAGGGTTAC-3′, and reverse, 5′-GATGTCTGGGTCTTGGTTCTC-3′; NLRP3 forward, 5′-AGCACCAGCCAGAGTCTAAC-3′, and reverse, 5′-CCCCAACCACAATCTCCGAAT-3′; ASC forward, 5′-AACCCAAGCAA GATGCGGAAG-3′, and reverse, 5′-TTAGGGCCTGGAGGAGCAAG-3′; Caspase-1 forward, 5′-CAAGGGTGCTGAACAAGG-3′, and reverse, 5′-GGGCATAGCTGGGTTGTC-3′; glyceraldehyde-3-phosphate dehydrogenase (GAPDH) forward, 5′-CATGTTCGTCATGGGTGTGA-3, and reverse, 5′-CAGGGGTGCTAAGCAGTTGG-3′ (Feria, Taborda, Hernandez, & Rugeles, 2018;Tzach-Nahman et al, 2017). Comparative quantification by PCR was performed with SYBR Premix Ex Taq using the Mx3000 P qPCR System (Agilent technologies, Santa Clara, CA).…”

Sulfur‑containing amino acids in aged garlic extract inhibit inflammation in human gingival epithelial cells by suppressing intercellular adhesion molecule‑1 expression and IL‑6 secretion

“…It has been demonstrated that excessive inflammation in the gingival tissue, as well as an immune reaction triggered by the increased number of periodontal pathogens, such as Porphyromonas gingivalis (P.g. ), plays an important role in the severity and progression of periodontal diseases (3,4). Thus, the control of inflammation may help to delay disease progression or recover severe symptoms in periodontal diseases.…”