Periodontal ligament fibroblasts migration injury via ROS/TXNIP/Nlrp3 inflammasome pathway with Porphyromonas gingivalis lipopolysaccharide

Lian, Dawei; Dai, Linfeng; Xie, Zhongjian; Xing, Zhimin; Liu, Xiaohong; Zhang, Yang; Huang, Yi; Chen, Yang

doi:10.1016/j.molimm.2018.10.001

Cited by 56 publications

(42 citation statements)

References 45 publications

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“…Recent studies have reported that oxidative stress is one of the main reasons for CNS dysfunction in MS [27]. ROS are the main mediators of oxidative stress and are initiators of the TXNIP/NLRP3 in ammasome [37][38][39]. In our study, we found that bixin attenuated ROS accumulation and downregulated the oxidative damage marker 3-NT in EAE mice.…”

Section: Discussionsupporting

confidence: 63%

Bixin Attenuates Experimental Autoimmune Encephalomyelitis by Suppressing TXNIP/NLRP3 inflammasome Activity and Activating Nrf2 Signaling

et al. 2020

Preprint

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Background Multiple sclerosis (MS), an autoimmune and degenerative disease, is characterized by demyelination and chronic neuroinflammation.Bixin is a carotenoid isolated from the seeds of Bixa orellana that exhibits various potent pharmacological activities, including antioxidant, anti-inflammation, and anti-tumor. However, the effects of bixin on MS remain elusive.Methods To evaluate the effects and underlying molecular mechanisms of bixin on MS, experimental autoimmune encephalomyelitis (EAE) was established in C57BL/6 mice, which were treated with intragastric administration of bixin solutions. To evaluate the molecular mechanisms of bixin, quantitative reverse-transcription PCR, western blot, immunohistochemistry, and enzyme-linked immunosorbent assay analyses were performed.Results We found that bixin significantly improved the symptoms in EAE mice, and suppressed microglia aggregation and TXNIP/NLRP3 inflammasome activity by scavenging excessive reactive oxygen species (ROS). Furthermore, bixin activated nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream genes in EAE mice, and these effects were suppressed upon inhibiting Nrf2 expression with the Nrf2 inhibitor ML385.Conclusions Bixin prevented neuroinflammation and demyelination in EAE mice mainly by scavenging ROS through activation of the Nrf2 signaling pathway. Taken together, our results indicate that bixin is a promising therapeutic candidate to treat MS.

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Section: Discussionsupporting

confidence: 63%

Bixin Attenuates Experimental Autoimmune Encephalomyelitis by Suppressing TXNIP/NLRP3 inflammasome Activity and Activating Nrf2 Signaling

et al. 2020

Preprint

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“…Moreover, we discovered that the content of LPS was significantly reduced after mixing P. gingivalis and L. reuteri sonicated extracts. L. reuteri not only has the main beneficial effect of Lactobacillus, it also has the ability to produce a broad spectrum of antimicrobial agent [40][41][42]. This substance, termed reuterin, has been reported to effectively inhibit the growth of harmful bacteria.…”

Section: Discussionmentioning

confidence: 99%

Balanced oral pathogenic bacteria and probiotics promoted wound healing via maintaining mesenchymal stem cell homeostasis

et al. 2020

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Objectives: The homeostasis of oral pathogenic bacteria and probiotics plays a crucial role in maintaining the well-being and healthy status of human host. Our previous study confirmed that imbalanced oral microbiota could impair mesenchymal stem cell (MSC) proliferation capacity and delay wound healing. However, the effects of balanced oral pathogenic bacteria and probiotics on MSCs and wound healing are far from clear. Here, the balance of pathogenic bacteria Porphyromonas gingivalis and probiotics Lactobacillus reuteri extracts was used to investigate whether balanced oral microbiota modulate the physiological functions of MSCs and promote wound healing. Methods: The effects of balanced pathogenic bacteria P. gingivalis and probiotics L. reuteri extracts on gingival MSCs (GMSCs) were tested using the migration, alkaline phosphatase activity, alizarin red staining, cell counting kit-8, realtime PCR, and western blot assays. To investigate the role of balanced pathogenic bacteria P. gingivalis and probiotics L. reuteri extracts in the wound of mice, the wounds were established in the mucosa of palate and were inoculated with bacteria every 2 days. Results: We found that the balance between pathogenic bacteria and probiotics enhanced the migration, osteogenic differentiation, and cell proliferation of MSCs. Additionally, local inoculation of the mixture of L. reuteri and P. gingivalis promoted the process of wound healing in mice. Mechanistically, we found that LPS in P. gingivalis could activate NLRP3 inflammasome and inhibit function of MSCs, thereby accelerating MSC dysfunction and delaying wound healing. Furthermore, we also found that reuterin was the effective ingredient in L. reuteri which maintained the balance of pathogenic bacteria and probiotics by neutralizing LPS in P. gingivalis, thus inhibiting inflammation and promoting wound healing. Conclusions: This study revealed that the homeostasis of oral microbiomes played an indispensable role in maintaining oral heath, provided hopeful methods for the prevention and treatment of oral diseases, and had some referential value for other systemic diseases caused by dysfunction of microbiota and MSCs.

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“…Functional consequences of NaB‐related morphological changes of mitochondria were a decrease of mitochondria membrane potential and impaired ATP production. Studies have shown that dysfunctional mitochondria release excessive ROS, which can activate inflammasomes and promote the occurrence of pyroptosis (Lian et al, ; Zhou, Yazdi, Menu, & Tschopp, ). Mitochondria damage is upstream or downstream of the NLRP3 and AIM2 inflammasomes (Allam et al, ; Zhou et al, ).…”

Section: Discussionmentioning

confidence: 99%

Butyrate rather than LPS subverts gingival epithelial homeostasis by downregulation of intercellular junctions and triggering pyroptosis

Liu

Wang

Meng

et al. 2019

J Clinic Periodontology

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Aim To investigate the effects of sodium butyrate (NaB) and lipopolysaccharide (LPS) on gingival epithelial barrier. Material and methods We cultured human primary gingival epithelial cells and investigated the effects of NaB and LPS on gingival epithelial barrier and involved mechanisms at in vitro and in vivo levels by immunostaining, confocal microscopy, field emission scanning electron microscopy (FE‐SEM), transmission electronic microscopy (TEM), transepithelial electrical resistance (TEER), FTIC‐dextran flux, flow cytometry, real‐time PCR and Western blot assays. Results Our results showed that NaB, rather than LPS, destroyed the epithelial barrier by breaking down cell–cell junctions and triggering gingival epithelial cell pyroptosis with characteristic morphological changes, including swollen cells, large bubbles, pore formation in the plasma membrane and subcellular organelles changes. The upregulated expression of pyroptosis‐related markers, caspase‐3 and gasdermin‐E (GSDME) contributed to this effect. Pyroptosis aroused by NaB is a pro‐inflammatory cell death. Pyroptotic cell death provoked inflammatory responses by upregulation of IL‐8 and MCP‐1, and releasing intracellular contents into the extracellular microenvironment after pyroptotic rupture of the plasma membrane. Conclusions Our new findings indicate that butyrate is a potent destructive factor of gingival epithelial barrier and pro‐inflammatory mediator, which shed a new light on our understanding of periodontitis initiation.

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Periodontal ligament fibroblasts migration injury via ROS/TXNIP/Nlrp3 inflammasome pathway with Porphyromonas gingivalis lipopolysaccharide

Cited by 56 publications

References 45 publications

Bixin Attenuates Experimental Autoimmune Encephalomyelitis by Suppressing TXNIP/NLRP3 inflammasome Activity and Activating Nrf2 Signaling

Bixin Attenuates Experimental Autoimmune Encephalomyelitis by Suppressing TXNIP/NLRP3 inflammasome Activity and Activating Nrf2 Signaling

Balanced oral pathogenic bacteria and probiotics promoted wound healing via maintaining mesenchymal stem cell homeostasis

Butyrate rather than LPS subverts gingival epithelial homeostasis by downregulation of intercellular junctions and triggering pyroptosis

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