Project description: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.
Project description:We have presented FROG and miniFROG reports for the first genome-scale model, iCJ415, for Streptococcus oralis SK141. The model can be found in the Supplementary Material of the publication by Jensen et al, 2020 cited here.
Project description:The human oral cavity harbors a diverse microbial community, with oral streptococci, particularly the Streptococcus mitis group, playing a pivotal role in biofilm formation and oral health. Among these, Streptococcus oralis is a key early colonizer that stabilizes oral biofilms. Here, we identify two mucin-degrading proteases, MdpS and MdpS2, that enable S. oralis to degrade MUC5B, the sole gel-forming mucin in saliva. Despite low sequence similarity, these enzymes share a high degree of tertiary structural resemblance and exhibits complementary biological functions. Their activity leads to extensive MUC5B degradation influencing biofilm dynamics by promoting biofilm dispersal and altering MUC5B and/or MUC5AC BCi mucus gels properties, with MdpS2 displaying specificity for MUC5B gels. Our findings reveal a specialized role in biofilm structural remodeling, offering potential avenues for clinical applications in biofilm modulation and mucus degradation.