Wnt5a is involved in LOX‐1 and TLR4 induced host inflammatory response in peri‐implantitis

Zhang, Qian; Liu, Jie; Ma, Lei; Bai, Na; Xu, Huilin

doi:10.1111/jre.12702

Cited by 25 publications

(23 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Studies have confirmed that Wnt5a can regulate a variety of inflammatory responses including the response to pulpitis [9,10,31,32]. In hDPC, Wnt5a can not only promote the upregulation of the expression of cytokines and chemokines induced by TNF-α but can also itself increase the levels of cytokines and chemokines in DPCs [10].…”

Section: Discussionmentioning

confidence: 92%

Wnt5a Regulates Odontoblast Inflammation by Promoting CCL2 Expression

Ge¹,

Huang²,

Zhao³

et al. 2021

Preprint

View full text Add to dashboard Cite

Objective Wnt5a is involved inflammation, including pulpitis, by upregulating cytokine/chemokine expression. Odontoblasts are the first layer cells in dental pulp and respond to inflammatory stimuli. However, whether Wnt5a is involved in odontoblast inflammation is unclear. This study aimed to investigate the role of Wnt5a in odontoblast inflammation. Methods We measured and compared Wnt5a- or TNF-α-induced cytokine/chemokine expression in mouse odontoblast-like (17IIA11) cells by real-time PCR and Western blotting. Transwell assays were used to examine the effect of Wnt5a on RAW264.7 macrophage migration. We examined whether the nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways were involved in the molecular mechanism of TNF-α or Wnt5a in 17IIA11 cells by Western blotting. Results TNF-α upregulated Wnt5a in odontoblasts. Wnt5a upregulated CCL2 expression in odontoblasts and enhanced RAW264.7 cell migration. We also found that TNF-α-induced Wnt5a expression was abrogated by inhibiting the MAPK pathway or NF-κB activity and that inhibiting MAPK activity could lead to decreased NF-κB activity. Conclusions Wnt5a is involved in the TNF-α-induced inflammatory response in odontoblasts. TNF-α upregulates Wnt5a expression via MAPK-dependent NF-κB activation in odontoblasts. Wnt5a upregulates CCL2 expression in odontoblasts and enhances RAW264.7 macrophage migration.

show abstract

Section: Discussionmentioning

confidence: 92%

Wnt5a Regulates Odontoblast Inflammation by Promoting CCL2 Expression

Ge¹,

Huang²,

Zhao³

et al. 2021

Preprint

View full text Add to dashboard Cite

show abstract

“…To investigate the immune responses associated with peri‐implantitis, most studies relied on studying the inflammatory tissue exudate (peri‐implant crevicular fluid PICF) 55 (Table 5). Soft tissue biopsies can give a more accurate account of the host molecular events 55 and some studies used gingival tissues to assess immune responses around dental implants 40,44,49 . The results from immune responses studies were conflicting, which could be due to the variability in microbiome composition, as described earlier, or as a result of different host responses to the peri‐implant infection between subjects.…”

Section: Discussionmentioning

confidence: 99%

“…Pro‐proinflammatory mediator IL‐1β, IL‐17, IL‐6, TNF‐α associated with peri‐implantitis appeared to be upregulated compared to healthy implants. Moreover, mediators that induce pro‐inflammatory cytokines (Wnt5a, HMGB1 and the antimicrobial effector HMGN2) were also upregulated in peri‐implantitis sites compared to healthy implants, although this is based on evidence from 1 study on each mediator 44,45 . The chemokines IL‐8 and the anti‐inflammatory mediators IL‐10 expression level is doubtful, as the disagreement between results is based on 2 studies only 39,40,42 …”

Section: Discussionmentioning

confidence: 99%

“…The anti‐inflammatory cytokine IL‐10 are highly expressed in the PICF of healthy implants in 1 study of 2 (50%) (Table 6). 39 Moreover, Wnt5a ligand that induce pro‐inflammatory cytokines was found to be expressed more in peri‐implantitis sites compared to healthy implants in 1 study (100%) 44 . Moreover, High Mobility Group Box 1 protein (HMGB1) and High Mobility Group Nucleosome‐binding protein (HMGN2) were expressed at higher levels in peri‐implantitis sites compared to healthy implants in 1 study 45 …”

Section: Human Immune Responsementioning

confidence: 96%

See 1 more Smart Citation

Microbiological Profile and Human Immune Response Associated with Peri‐Implantitis: A Systematic Review

Kensara

Hefni

Williams

et al. 2020

Journal of Prosthodontics

View full text Add to dashboard Cite

Purpose To evaluate and synthesize the existing evidence on the microbiological and human immune response associated with peri‐implantitis in comparison to healthy implants. Materials and methods Three electronic databases (MEDLINE, Embase, and Cochrane Library) were searched in October 2019 to identify clinical studies evaluating the microbiota and the immune response associated with peri‐implantitis. Two reviewers independently screened the studies and used the full text to extract the data. A qualitative synthesis was performed on the extracted data and summary tables were prepared. Due to clinical and methodological heterogeneity among included studies, no meta‐analysis was performed. Results Forty studies were included in this review. Of these, 20 studies compared the microbiological profile of peri‐implantitis with healthy implants. Nineteen studies focused on the immune response associated with peri‐implantitis in comparison to healthy implants. Three studies focus on gene polymorphism associated with peri‐implantitis. The most commonly reported bacteria associated with peri‐implantitis were obligate anaerobe Gram‐negative bacteria (OAGNB), asaccharolytic anaerobic Gram‐positive rods (AAGPRs), and other Gram‐positive species. In regard to immune response, the most frequently reported pro‐inflammatory mediators associated with peri‐implantitis were IL‐1β, IL‐6, IL‐17, TNF‐α. Osteolytic mediator, e.g., RANK, RANKL, Wnt5a and proteinase enzymes, MMP‐2, MMP‐9, and Cathepsin‐K were also expressed at higher level in peri‐implantitis sites compared to control. Conclusions Peri‐implantitis is associated with complex and different microbiota than healthy implants including bacteria, archaea, fungi, and virus. This difference in the microbiota could provoke higher inflammatory response and osteolytic activity. All of this could contribute to the physiopathology of peri‐implantitis.

show abstract

“…Wnt5a has been demonstrated to regulate inflammatory cytokines and to aggravate the destruction of periodontium. Inhibition of Wnt5a by small interfering (si)RNA or a neutralizing antibody significantly reduced the expression of interleukin (IL)-1β, monocyte chemotactic protein 1, and matrix metalloproteinase 2 in P. gingivalis -infected macrophages ( 45 ). Local administration of exogenous Wnt5a in the gingiva of mice with ligature-induced periodontitis exacerbated alveolar bone loss ( 40 ).…”

Section: Wnt5a In Periodontitismentioning

confidence: 99%