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Effects of Streptococcus oralis biofilm on peri-implant soft-tissue cells

ABSTRACT: Human gingival epithelial cells (HGEp) and fibroblasts (HGF) are the main cell types of the peri-implant soft-tissue, with HGEp constantly being exposed to bacteria and HGF residing protected in the connective tissue as long as an intact mucosa-implant seal is preserved. Streptococcus oralis belongs to the commensal bacteria, is highly abundant at healthy implant sites, and might exert host modulatory effects on soft-tissue cells as described for other streptococci. Thus, we aimed to investigate the effects of S. oralis biofilm on HGEp as well as HGF. HGEp or HGF were grown on titanium separately and responded to S. oralis biofilm challenge. The cell condition of HGF was dramatically impaired after 4 hours showing a transcriptional inflammatory and stress response. In contrast, S. oralis challenge induced only transcriptional inflammatory response in HGEp with their cell condition remaining unaffected. Subsequently, HGF were susceptible compared to HGEp. The proinflammatory IL-6 was attenuated in HGF and CXCL8 in HGEp indicating a general tissue-protective role of S. oralis, forasmuch as the HGF are not exposed. In conclusion, an intact implant-mucosa interface is a prerequisite so that commensal biofilms can promote homeostasis for tissue protection.

ORGANISM(S): Homo sapiens

PROVIDER: GSE134481 | GEO | 2020/06/17

REPOSITORIES: GEO

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Project description:Oral health is associated with a symbiotic microbial community and host-microbe homeostasis is maintained by the controlled immune response. Various factors can disrupt this homeostasis. Dysbiosis, which is characterized by increased immune response and a shift in the microbiome, contributes the pathogenesis of peri-implantitis. Peri-implant mucosa and commensal bacteria play important roles in the maintenance of host-microbe homeostasis, but little is known about how they interact. We have therefore investigated the early host-microbe interaction between a commensal multispecies biofilm (Streptococcus oralis, Actinomyces naeslundii, Veillonella dispar, Porphyromonas gingivalis) and peri-implant mucosa at 24 and 48 h. Our in vitro peri-implant mucosa-biofilm model contained organotypic oral mucosa, implant material and biofilm. After 24 h, the biofilm induced a modest innate immune response in the peri-implant mucosa by the upregulation of 5 genes related to immune and inflammatory response and the increased secretion of IL-6 and CCL20. This controlled immune response protected tissue integrity and the peri-implant mucosa remained intact. The secreted antibacterial proteins human β-Defensins-1, -2, and CCL20 controlled the overgrowth of the biofilm by reducing its volume - without affecting the live/dead ratio or bacterial distribution. Thus, host-microbe homeostasis was established within the first 24 h. In contrast, host-microbe homeostasis was disrupted after 48 h. The mucosa was damaged and detached from the implant, due to the induced downregulation of cell adhesion related genes. The immune response was enhanced by upregulation of additional genes related to the immune and inflammatory response and increased secretion of IL-1β, TNF-α, and CCL20. Moreover, bacterial distribution was altered, with an increased proportion of V. dispar. The disrupted host-microbe homeostasis could lead to incipient dysbiosis. This deeper understanding of the early host-microbe interaction at the peri-implant site may provide the basis for new strategies to improve the prevention and therapy of peri-implant diseases.

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Effects of Streptococcus oralis biofilm on peri-implant soft-tissue cells

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