Chemerin contributes to inflammatory responses and suppresses osteogenic differentiation in chronic periodontitis

Oral Diseases ◽  
2022 ◽  
Author(s):  
Xinling Wang ◽  
Yuejun Tang ◽  
Rui Xiao
Keyword(s):  
Osteogenic Differentiation ◽  
Chronic Periodontitis ◽  
Inflammatory Responses

scholarly journals Oral Mucosal Endotoxin Tolerance Induction in Chronic Periodontitis

2005 ◽  
Vol 73 (2) ◽  
pp. 687-694 ◽  
Author(s):  
Manoj Muthukuru ◽  
Ravi Jotwani ◽  
Christopher W. Cutler
Keyword(s):  
Immune Response ◽  
Oral Mucosa ◽  
Chronic Periodontitis ◽  
Intracellular Signaling ◽  
Inflammatory Responses ◽  
Endotoxin Tolerance ◽  
Necrosis Factor Alpha ◽  
Initial Stimulus ◽  
Tlr4 Mrna ◽  
Tnf Α

ABSTRACT The oral mucosa is exposed to a high density and diversity of gram-positive and gram-negative bacteria, but very little is known about how immune homeostasis is maintained in this environment, particularly in the inflammatory disease chronic periodontitis (CP). The cells of the innate immune response recognize bacterial structures via the Toll-like receptors (TLR). This activates intracellular signaling and transcription of proteins essential for the induction of an adaptive immune response; however, if unregulated, it can lead to destructive inflammatory responses. Using single-immunoenzyme labeling, we show that the human oral mucosa (gingiva) is infiltrated by large numbers of TLR2+ and TLR4+ cells and that their numbers increase significantly in CP, relative to health (P < 0.05, Student's t test). We also show that the numbers of TLR2+ but not TLR4+ cells increase linearly with inflammation (r 2 = 0.33, P < 0.05). Double-immunofluorescence analysis confirms that TLR2 is coexpressed by monocytes (MC)/macrophages (mφ) in situ. Further analysis of gingival tissues by quantitative real-time PCR, however, indicates that despite a threefold increase in the expression of interleukin-1β (IL-1β) mRNA during CP, there is significant (30-fold) downregulation of TLR2 mRNA (P < 0.05, Student's t test). Also showing similar trends are the levels of TLR4 (ninefold reduction), TLR5 (twofold reduction), and MD-2 (sevenfold reduction) mRNA in CP patients compared to healthy persons, while the level of CD14 was unchanged. In vitro studies with human MC indicate that MC respond to an initial stimulus of lipopolysaccharide (LPS) from Porphyromonas gingivalis (PgLPS) or Escherichia coli (EcLPS) by upregulation of TLR2 and TLR4 mRNA and protein; moreover, IL-1β mRNA is induced and tumor necrosis factor alpha (TNF-α), IL-10, IL-6, and IL-8 proteins are secreted. However, restimulation of MC with either PgLPS or EcLPS downregulates TLR2 and TLR4 mRNA and protein and IL-1β mRNA and induces a ca. 10-fold reduction in TNF-α secretion, suggesting the induction of endotoxin tolerance by either LPS. Less susceptible to tolerance than TNF-α were IL-6, IL-10, and IL-8. These studies suggest that certain components of the innate oral mucosal immune response, most notably TLRs and inflammatory cytokines, may become tolerized during sustained exposure to bacterial structures such as LPS and that this may be one mechanism used in the oral mucosa to attempt to regulate local immune responses.

scholarly journals Single-Cell RNA Sequencing Identifies New Inflammation-Promoting Cell Subsets in Asian Patients With Chronic Periodontitis

2021 ◽  
Vol 12 ◽  
Author(s):  
Shu-jiao Qian ◽  
Qian-ru Huang ◽  
Rui-ying Chen ◽  
Jia-ji Mo ◽  
Lin-yi Zhou ◽  
...  
Keyword(s):  
Single Cell ◽  
Chronic Periodontitis ◽  
Inflammatory Responses ◽  
Cell Communication ◽  
Cell Types ◽  
Chronic Inflammatory Disease ◽  
Periodontal Tissues ◽  
Asian Patients ◽  
Healthy Donors ◽  
Human Gingiva

Periodontitis is a highly prevalent chronic inflammatory disease leading to periodontal tissue breakdown and subsequent tooth loss, in which excessive host immune response accounts for most of the tissue damage and disease progression. Despite of the imperative need to develop host modulation therapy, the inflammatory responses and cell population dynamics which are finely tuned by the pathological microenvironment in periodontitis remained unclear. To investigate the local microenvironment of the inflammatory response in periodontitis, 10 periodontitis patients and 10 healthy volunteers were involved in this study. Single-cell transcriptomic profilings of gingival tissues from two patients and two healthy donors were performed. Histology, immunohistochemistry, and flow cytometry analysis were performed to further validate the identified cell subtypes and their involvement in periodontitis. Based on our single-cell resolution analysis, we identified HLA-DR-expressing endothelial cells and CXCL13+ fibroblasts which are highly associated with immune regulation. We also revealed the involvement of the proinflammatory NLRP3+ macrophages in periodontitis. We further showed the increased cell-cell communication between macrophage and T/B cells in the inflammatory periodontal tissues. Our data generated an intriguing catalog of cell types and interaction networks in the human gingiva and identified new inflammation-promoting cell subtypes involved in chronic periodontitis, which will be helpful in advancing host modulation therapy.

scholarly journals Lack of Association between Interleukin-1βGene Polymorphism (rs16944) and Chronic Periodontitis: From a Case-Control Studies to an Updated Meta-Analysis

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Seoung-Jin Hong ◽  
Sang Wook Kang ◽  
Su Kang Kim ◽  
Young Sik Kim ◽  
Ju Yeon Ban
Keyword(s):  
Chronic Periodontitis ◽  
Case Control Study ◽  
Inflammatory Responses ◽  
Direct Sequencing ◽  
Meta Analysis ◽  
Interleukin 1 ◽  
Information Service ◽  
Case Control ◽  
Case Control Studies ◽  
Control Study

Background. Interleukin-1β(IL-1β) plays an important role as a mediator of various inflammatory responses in chronic periodontitis. Several studies have investigated the potential relationship between IL-1βpolymorphism (rs16944) and susceptibility to chronic periodontitis; inflammatory process is involved, but conclusions is still controversial.Objective. The aim of this study was to determine whether the IL-1βpolymorphism (rs16944) is associated with susceptibility to chronic periodontitis.Material and Methods. For the case-control study, 51 patients with chronic periodontitis and 33 healthy control patients were recruited in the study. Genotyping was conducted by direct sequencing. SNPStats and SPSS 18.0 were used for the analysis of genetic data and to evaluate odds ratios, 95% confidence intervals, andPvalues; logistic regression models were used. And to perform meta-analysis, studies about IL-1βpolymorphism (rs16944) and chronic periodontitis were searched in PubMed, Embase, Google Scholar, and Korean Studies Information Service System (KISS) electronic databases until July 2017.Results. In our case-control study, no significant relationship was revealed between IL-1βpolymorphism (rs16944) and chronic periodontitis (P>0.05in each model). When combined with the previous studies in the meta-analysis, the result was not associated with chronic periodontitis in any of the models (CC vs. CT + TT: OR = 0.97, 95% CI = 0.762–1.246; CC + CT vs. TT: OR = 0.90, 95% CI = 0.658–1.232; and C vs. T: OR = 0.93, 95% CI = 0.774–1.128). The subgroup analysis stratified by ethnicity showed a weak association between the IL-1βpolymorphism (rs16944) and chronic periodontitis in the Caucasian population (recessive model, OR = 1.34, 95% CI = 1.017–1.758,P=0.037).Conclusion. Evidences from a case-control study and the meta-analysis suggest that IL-1βpolymorphism (rs16944) is not associated with susceptibility to chronic periodontitis.

scholarly journals Systemic inflammatory responses in patients with type 2 diabetes with chronic periodontitis

2016 ◽  
Vol 4 (1) ◽  
pp. e000260 ◽  
Author(s):  
Ruben Mesia ◽  
Fatemeh Gholami ◽  
Hong Huang ◽  
Michael Clare-Salzler ◽  
Ikramuddin Aukhil ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Chronic Periodontitis ◽  
Inflammatory Responses

Attenuation of Porphyromonas Gingival Lipopolysaccharide-Induced Periodontal Ligament Stem Cells Injury and Inflammation by Blocking Cell Pyroptosis

2021 ◽  
Vol 11 (10) ◽  
pp. 1940-1946
Author(s):  
Shuangfeng Jiang ◽  
Shanjuan Huang ◽  
Jin Liu ◽  
Qi Zhou ◽  
Xiaosheng Liu
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Osteogenic Differentiation ◽  
Inflammatory Cytokines ◽  
Chronic Periodontitis ◽  
Cell Apoptosis ◽  
Periodontal Ligament ◽  
High Mobility ◽  
Periodontal Ligament Stem Cells ◽  
Alizarin Red

Periodontitis is a chronic inflammation of periodontal tissue, and programmed cell death plays an important role in chronic periodontitis induced by P. gingivalis. Studies have shown that the increased expression of pyroptosis-related NLRP3 inflammasome and the pro-inflammatory cytokines IL-1β and IL-18 in gingivitis, invasive periodontitis, and chronic periodontitis patients. The present study aimed to investigate whether the inhibition of pyroptosis could protect porphyromonas gingival lipopolysaccharide (pg-LPS)-induced human periodontal ligament stem cells (hPDLSCs) injury and inflammation. The hPDLSCs were treated with pg-LPS and ATP in the presence of caspase1/4 inhibitor VX765. The cell proliferation and survival were assessed by CCK-8, the osteogenic differentiation capacity was evaluated by Alkaline Phosphatase (ALP) assay and alizarin red staining. Then, cell apoptosis, cleavage of gasdermin D (GSDMD) and generation of inflammatory cytokines were estimated. Lastly, western blotting was used to detect the expression of potential target proteins. Results showed that the treatment of pg-LPS plus ATP significantly inhibited the proliferation, survival and osteogenic differentiation of hPDLSCs, while inducing cell apoptosis, pyroptosis and inflammation. However, the presence of VX765 partially recovered the cell proliferation, survival and osteogenic differentiation. At the same time, VX765 inhibited cell apoptosis, cleavage of GSDMD and generation of inflammatory cytokines. Besides, the expression of related proteins including Bax, Bcl-2, cleaved (c)-caspase3, c-caspase4, c-caspase1, Toll Like Receptor 4, High Mobility Group Box 1 (HMGB1) and NLRP3 was all rescued by VX765. In conclusion, our results revealed that the blocking of cell pyroptosis could protect hPDLSCs from pg-LPS-induced injury. Therefore, the application of pyroptosis inhibitor may be a valuable therapeutic approach for treating periodontitis.

scholarly journals GABARAP ameliorates IL-1β-induced inflammatory responses and osteogenic differentiation in bone marrow-derived stromal cells by activating autophagy

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xiaobo Guo ◽  
Zhenyuan Wu
Keyword(s):  
Osteogenic Differentiation ◽  
Inflammatory Responses ◽  
Interleukin 1 ◽  
Inflammatory Factors ◽  
Ros Generation ◽  
Protective Effects ◽  
Bone Mesenchymal Stem Cells ◽  
Alizarin Red ◽  
Expression Levels

AbstractBone mesenchymal stem cells (BMSCs) are the most commonly investigated progenitor cells in bone defect repair and osteoarthritis subchondral bone regeneration; however, these studies are limited by complex inflammatory conditions. In this study, we investigated whether pro-autophagic γ-aminobutyric acid receptor-associated protein (GABARAP) promotes BMSCs proliferation and osteogenic differentiation by modulating autophagy in the presence or absence of interleukin-1 beta (IL-1β) in vitro. The expression levels of all relevant factors were evaluated by qRT-PCR or western blotting where appropriate. BMSCs differentiation were assessed by Alizarin Red, alkaline phosphatase, safranin O, and Oil Red O staining. Furthermore, the interactions between autophagy and osteogenic differentiation were investigated by co-treatment with the autophagy inhibitor 3-methyladenine (3-MA). As the results, we found that treatment with recombinant human His6-GABARAP protein promoted cell proliferation, inhibited apoptosis, and reduced ROS generation by increasing autophagic activity, particularly when co-cultured with IL-1β. Moreover, His6-GABARAP could effectively increase the osteogenic differentiation of BMSCs. The expression levels of inflammatory factors were significantly decreased by His6-GABARAP treatment, whereas its protective effects were attenuated by 3-MA. This study demonstrates that GABARAP maintains BMSCs survival and strengthens their osteogenic differentiation in an inflammatory environment by upregulating mediators of the autophagy pathway.

5,7-Dihydroxyflavone analogues may regulate lipopolysaccharide-induced inflammatory responses by suppressing IκBα-linked Akt and ERK5 phosphorylation in RAW 264.7 macrophages

Planta Medica ◽  
2016 ◽  
Vol 81 (S 01) ◽  
pp. S1-S381
Author(s):  
A Nishina ◽  
M Ukiya ◽  
M Fukatsu ◽  
M Koketsu ◽  
M Ninomiya ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Raw 264.7 ◽  
Raw 264.7 Macrophages
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