Epithelial cell pro‐inflammatory cytokine response differs across dental plaque bacterial species

Abstract

Aim-The dental plaque is comprised of numerous bacterial species which may or may not be pathogenic. Human gingival epithelial cells (HGECs) respond to perturbation by various bacteria of the dental plaque by production of different levels of inflammatory cytokines which is a putative reflection of their virulence. The aim of the current study was to determine responses in terms of IL-1β, IL-6, IL-8 and IL-10 secretion induced by Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Fusobacterium nucleatum and Streptococcus gordonii in order to gauge their virulence potential.Materials and Methods-HGECs were challenged with the four bacterial species, live or heatkilled, at various MOIs (multiplicity of infection) and the elicited IL-1β, IL-6, IL-8 and IL-10 responses were assayed by ELISA. Results-PrimaryHGECs challenged with live P. gingivalis produced high levels of IL-1β, while challenge with live A. actinomycetemcomitans gave high levels of IL-8. The opportunistic pathogen F. nucleatum induces the highest levels of pro-inflammatory cytokines, while the commensal S. gordonii is the least stimulatory.Conclusion-We conclude that various dental plaque biofilm bacteria induce different cytokine response profiles in primary human gingival epithelial cells that may reflect their individual virulence or commensal status.

Oral Epithelial Cell Responses to Multispecies Microbial Biofilms

“…Extensive results have documented the responses of epithelial cells after challenge with planktonic oral bacteria (Huang et al, 2004;Hasegawa et al, 2007;Ji et al, 2007;Stathopoulou et al, 2010). However, current models of the host-microbe interactions in the oral cavity emphasize the critical nature of complex microbial biofilms that form unique microbial ecologies (Colombo et al, 2009;Darveau, 2009) and that change during transition from health to disease (Marsh, 2010).…”

“…A range of gingival cells responds to this microbial challenge in the oral cavity (Kebschull and Papapanou, 2011). To maintain homeostasis, these responses have evolved with pro-and antiinflammatory molecules and cell communication molecules arising from the resident cells of the periodontium (Bodet et al, 2006;Stathopoulou et al, 2010). Additional molecules derive from infiltrating inflammatory and immune cells in the affected tissues.…”

“…Historically, most in vitro studies have evaluated how individual planktonic bacteria or their component products would trigger host responses (Ji et al, 2007;Stathopoulou et al, 2010). The investigations were designed to identify specific response molecules (Ji et al, 2007;Mans et al, 2009), as well as the receptors and ligand interactions that account for the responses (Hayashi et al, 2010).…”

Inflammatory Bone Loss in Experimental Periodontitis Induced by Aggregatibacter actinomycetemcomitans in Interleukin-1 Receptor Antagonist Knockout Mice

“…Mice were infected a total of 5 times at 1-day intervals. Forty-two days after the last infection, blood was collected from the inferior vena cava, and sera were obtained; mandibles were removed and immediately fixed in 4% paraformaldehyde overnight at 4°C, and then micro-computed tomography (micro-CT) analysis was performed (27,28).…”

TLR2 Promoter Hypermethylation Creates Innate Immune Dysbiosis

“…2A). The time points for this chronic infection were carefully chosen based on our previously published results on P. gingivalisinduced inflammatory cytokine response in gingival epithelial cells (Eskan et al 2008;Stathopoulou et al 2009;Stathopoulou et al 2010). By using this method, we successfully induced tolerance to P. gingivalis (live bacteria at MOI: 5) in normal epithelial cells.…”