Streptococcus oralis coaggregation receptor polysaccharides induce inflammatory responses in human aortic endothelial cells

Abstract

Summary Streptococcus oralis, belonging to the oral viridans group streptococci, has been detected in human cardiovascular lesions including infective endocarditis and atheromatous plaques. The organism has coaggregation receptor polysaccharides (RPS) on the cell wall, which function as receptors for surface adhesins on other members of the oral biofilm community. The present study examined the capacity of S. oralis RPS to induce inflammatory responses in human aortic endothelial cells (HAECs). Purified RPS was used to stimulate HAECs, and the induction of cytokines, adhesion molecules and Toll‐like receptors (TLRs) was examined. Involvement of RPS in HAEC invasion by S. oralis was also examined. RPS‐stimulated HAECs produced more cytokines (interleukin‐6, interleukin‐8 and monocyte chemoattractant protein‐1) and intercellular adhesion molecule‐1 than non‐stimulated HAECs. The messenger RNA (mRNA) expression of cytokines and adhesion molecules in RPS‐stimulated HAECs increased markedly compared with that in non‐stimulated HAECs. Upregulation of TLR‐2 mRNA expression was demonstrated in RPS‐stimulated HAECs. Moreover, TLR‐2 mRNA expression and cytokine production were reduced by the incubation of HAECs with inhibitors against p38 mitogen‐activated protein kinase and nuclear factor‐κB. An RPS‐defective mutant of S. oralis showed greater invasion into HAECs than an RPS‐possessing strain. However, HAECs invaded by the RPS‐defective mutant produced less cytokines than HAECs invaded by the RPS‐possessing strain, indicating that RPS can stimulate HAECs intracellularly. These results suggest that S. oralis RPS may be an important contributor to the pathogenesis of cardiovascular diseases such as infective endocarditis and atherosclerosis.

Mature Biofilm Degradation by Potential Probiotics: Aggregatibacter actinomycetemcomitans versus Lactobacillus spp.

“…This suggests that the activity was not nutrient-dependent and that direct cell contact was possibly a physical factor that contributed to biofilm degradation. In theory, a co-aggregation between cells will contribute to a higher biofilm formation [ 54 , 55 ]. This phenomenon was observed with dead probiotic cells against the pre-formed biofilm.…”

Colonisation of gingival epithelia by subgingival biofilms in vitro: Role of “red complex” bacteria

“…Two streptococcal species are included in the composition of the present 10-species biofilm model, namely S. oralis and S. anginosus. There is evidence that planktonic cultures of S. oralis can invade in vitro monolayers of human umbilical vein endothelial cells (HUVEC)27 , or human aortic endothelial cells (HAECs)28,29 , whereas S. anginosus has a very restricted invasive capacity29 . To date there is no evidence of the colonization capacity of these two streptococci on gingival epithelial cells, neither in planktonic state, nor as part of multispecies biofilms.…”

Secreted products of oral bacteria and biofilms impede mineralization of apical papilla stem cells in TLR-, species-, and culture-dependent fashion

“…Indeed, exposure to S. oralis products had detrimental effects on the basic cell processes and the mineralizing efficiency of SCAPs. For this specific bacterial species, surface components (other than the frequently reported LTA and peptidoglycans) involved to bacterial adhesion and colonization events might have contributed to this considerably high TLR2 gene expression and the inflammatory SCAPs polarization observed 44 , 45 . Interestingly, A. naeslundii T14V-J1 products led only to a minor decline.…”