The virulence factor GroEL promotes gelatinase secretion from cells in the osteoblast lineage: Implication for direct crosstalk between bacteria and adult cells

Zhang, Li; Cui, Yujia; Yang, Yueyi; Wei, Jieya; Liu, Wenjing; Cai, Lu; Wang, Luling; Zhang, Demao; Xie, Jing; Cheng, Lei

doi:10.1016/j.archoralbio.2020.104991

Cited by 7 publications

(3 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“… 103 P. gingivalis further secretes gingipains to promote the activation of proMMP9 and form active MMP9, which participates in the destruction of the surrounding matrix of the cell, promotes the inflammation and the invasion and metastasis of OSCC cells. 104 Gingipains can exert cytotoxic effects, stimulate host endothelial cells to secrete IL-8, promote tumor angiogenesis and tumor growth, and change T cell functions by degrading T cell surface receptors and enhance OSCC immune escape. 105 …”

Section: Oral Bacteria and Cancersmentioning

confidence: 99%

Oral microbiota in human systematic diseases

et al. 2022

Self Cite

View full text Add to dashboard Cite

Oral bacteria directly affect the disease status of dental caries and periodontal diseases. The dynamic oral microbiota cooperates with the host to reflect the information and status of immunity and metabolism through two-way communication along the oral cavity and the systemic organs. The oral cavity is one of the most important interaction windows between the human body and the environment. The microenvironment at different sites in the oral cavity has different microbial compositions and is regulated by complex signaling, hosts, and external environmental factors. These processes may affect or reflect human health because certain health states seem to be related to the composition of oral bacteria, and the destruction of the microbial community is related to systemic diseases. In this review, we discussed emerging and exciting evidence of complex and important connections between the oral microbes and multiple human systemic diseases, and the possible contribution of the oral microorganisms to systemic diseases. This review aims to enhance the interest to oral microbes on the whole human body, and also improve clinician’s understanding of the role of oral microbes in systemic diseases. Microbial research in dentistry potentially enhances our knowledge of the pathogenic mechanisms of oral diseases, and at the same time, continuous advances in this frontier field may lead to a tangible impact on human health.

show abstract

Section: Oral Bacteria and Cancersmentioning

confidence: 99%

Oral microbiota in human systematic diseases

et al. 2022

Self Cite

View full text Add to dashboard Cite

show abstract

“…For example, GroEL upregulated the secretion of cytokines in human periodontal ligament (PDL) cells, human gingival fibroblasts and osteoblasts, potentially via NF‐κB activation 8–10 . Our previous study also illustrated that GroEL can stimulate osteoblasts to boost gelatinase secretion 11 . However, the potential mechanisms of the GroEL‐host interaction are not completely clear.…”

Section: Introductionmentioning

confidence: 98%

“…[8][9][10] Our previous study also illustrated that GroEL can stimulate osteoblasts to boost gelatinase secretion. 11 However, the potential mechanisms of the GroEL-host interaction are not completely clear.…”

Section: Introductionmentioning

confidence: 99%

The virulence factor GroEL directs the osteogenic and adipogenic differentiation of human periodontal ligament stem cells through the involvement of JNK/MAPK and NF‐κB signaling

Zhang

Cheng

Cui

et al. 2021

Journal of Periodontology

Self Cite

View full text Add to dashboard Cite

Background GroEL, a bacterial metabolite, is an important stimulator of inflammation. The aim of this study is to confirm the effect of the virulence factor GroEL on differentiation potential of periodontal ligament (PDL) stem cells (PDLSCs) and the potential mechanisms. Methods PDLSCs were obtained from extracted human premolars. GroEL was administered to osteogenic‐ and adipogenic‐induced hPDLSCs. Alkaline phosphatase (ALP) staining, Alizarin Red staining and Oil Red staining were performed. Gene and protein expression were separately measured by qPCR and Western blotting. The expression and localization of activated signaling factors were confirmed by immunofluorescence staining. The inhibitors of myeloid differentiation factor 88 (MyD88, an adaptor protein of TLRs), JNK/MAPK and NF‐κB signaling were used to verify their specific effects. Results First, we found that GroEL inhibited the osteogenic differentiation and enhanced the adipogenic differentiation of hPDLSCs. Next, we found that GroEL increased the expression of TLR2 and TLR4 and GroEL activated JNK/MAPK and NF‐κB signaling, which can be blocked by inhibition of MyD88. Finally, we found that inhibition of MyD88 restored GroEL‐induced osteogenic and adipogenic differentiation and blocking JNK/MAPK or NF‐κB signaling partly restored GroEL effects. Conclusion In the current study, we revealed a potential interaction between bacteria and host cells by showing that GroEL directs the osteogenic and adipogenic differentiation of hPDLSCs by the involvement of JNK/MAPK and NF‐κB signaling. This study provides evidence that bacterial products can influence the differentiation of stem cells and reveals potential effect of GroEL on the context of tissue regeneration.

show abstract

Outer Membrane Vesicles Derived From Fusobacterium nucleatum Trigger Periodontitis Through Host Overimmunity

Zhang,

Liu

et al. 2024

Advanced Science

View full text Add to dashboard Cite

The virulent bacteria‐induced host immune response dominates the occurrence and progression of periodontal diseases because of the roles of individual virulence factors from these pathogens in the initiation and spread of inflammation. Outer membrane vesicles (OMVs) as a pathogenic entity have recently attracted great attention as messenger bridges between bacteria and host tissues. Herein, the novel role of OMVs derived from Fusobacterium nucleatum in the occurrence of periodontitis is dissected. In a rat periodontitis model, it is found that OMVs derived from F. nucleatum caused deterioration of periodontitis by enhancing inflammation of the periodontium and absorption of alveolar bone, which is almost equivalent to the effect of F. nucleatum itself. Furthermore, that OMVs can independently induce periodontitis is shown. The pathogenicity of OMVs is attributed to multiple pathogenic components identified by omics. After entering human periodontal ligament stem cells (hPDLSCs) by endocytosis, OMVs activated NLRP3 inflammasomes and impaired the mineralization of hPDLSCs through NF‐κB (p65) signaling, leading to the final injury of the periodontium and damage of alveolar bone in periodontitis. These results provide a new understanding of OMVs derived from pathogens and cues for the prevention of periodontitis.

show abstract

The virulence factor GroEL promotes gelatinase secretion from cells in the osteoblast lineage: Implication for direct crosstalk between bacteria and adult cells

Cited by 7 publications

References 57 publications

Oral microbiota in human systematic diseases

Oral microbiota in human systematic diseases

The virulence factor GroEL directs the osteogenic and adipogenic differentiation of human periodontal ligament stem cells through the involvement of JNK/MAPK and NF‐κB signaling

Outer Membrane Vesicles Derived From Fusobacterium nucleatum Trigger Periodontitis Through Host Overimmunity

Contact Info

Product

Resources

About