Enterococcus faecalis Lipoteichoic Acid–induced NLRP3 Inflammasome via the Activation of the Nuclear Factor Kappa B Pathway

Wang, Lina; Jin, Hui‐Zi; Ye, Dandan; Wang, Jiaojiao; Ao, Xiang; Dong, Ming; Niu, Weidong

doi:10.1016/j.joen.2016.04.018

Cited by 34 publications

(31 citation statements)

References 35 publications

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“…Abundant research indicated that S. aureus LTA could induce TLR2 activation and subsequently lead to the stimulation of NF-κB signaling and NLRP3 [7,8]. The NLRP3 inflammasome is tightly controlled by a priming step that is dependent on NF-κB and is highly inducible in response to pro-inflammatory stimuli such as S. aureus LTA [9]. The NLRP3 inflammasome consists of NLRP3, apoptosis-associated speck-like protein containing CARD (ASC), and pro-caspase-1, which influences the regulation of pro-inflammatory cytokine secretion, particularly the generation of interleukin 1 beta (IL-1β) [10].…”

Section: Introductionmentioning

confidence: 99%

Sodium Phenylbutyrate Ameliorates Inflammatory Response Induced by Staphylococcus aureus Lipoteichoic Acid via Suppressing TLR2/NF-κB/NLRP3 Pathways in MAC-T Cells

et al. 2018

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This study aimed to investigate the anti-inflammatory properties of sodium phenylbutyrate (SPB) against Staphylococcus aureus (S. aureus) lipoteichoic acid (LTA)-stimulated bovine mammary alveolar (MAC-T) cells. Quantitative PCR was performed to examine the effect of SPB on inflammatory cytokines and host defense peptide (HDP) gene expression. Western blot wanalysis was used to detect the effect of SPB on the TLR2/NF-κB/NLRP3 signaling pathway. The results showed that SPB significantly suppressed the expression of TNF-α, IL-1β, IL-6; meanwhile, the markedly decreased expression of LTA-stimulated TLR2, NLRP3, ASC, caspase-1, and IL-1β, and the inhibited IkBα and p65 phosphorylation were also observed. However, increased TAP and Bac5 expression in LTA-stimulated MAC-T cells was further detected. In summary, these results suggest that SPB ameliorates the inflammatory response induced by S. aureus LTA via suppressing the TLR2/NF-κB/NLRP3 signaling pathway, which indicates that SPB may be a potential agent for the treatment of bovine mastitis.

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Section: Introductionmentioning

confidence: 99%

Sodium Phenylbutyrate Ameliorates Inflammatory Response Induced by Staphylococcus aureus Lipoteichoic Acid via Suppressing TLR2/NF-κB/NLRP3 Pathways in MAC-T Cells

et al. 2018

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“…When inflammation progressed in the fourth week, bone resorption was chronic. Compared with the previous establishment of rat apical periodontitis [15–17], establishment of the mouse apical periodontitis animal model was more complicated but was feasible as many transgenic mouse models are used in research. This study successfully established a mouse model of apical periodontitis to provide a basis for further study of the mechanism of apical periodontitis in transgenic mice.…”

Section: Discussionmentioning

confidence: 99%

Role of the Btk-PLCγ2 Signaling Pathway in the Bone Destruction of Apical Periodontitis

Wang

Zhang

Dong

et al. 2019

Mediators of Inflammation

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Chronic apical periodontitis is characterized by alveolar bone absorption in the apical region and is the result of the participation of various inflammatory mediators. Studies have shown that the Bruton tyrosine kinase- (Btk-) phospholipase Cγ2 (PLCγ2) signaling pathway plays an important role in bone absorption, but it is unknown whether it plays a role in apical periodontitis bone destruction. Therefore, this study verified the role of Btk and PLCγ2 in bone resorption of apical periodontitis by in vivo and in vitro experiments. In the in vivo experiment, a mice model of apical periodontitis was established; apical bone resorption was confirmed by the numbers of osteoclasts and HE staining. Btk, PLCγ2, and nuclear factor of activated T-cells 1 (NFATc-1) were detected by immunohistochemical staining. In the in vitro experiment, lipopolysaccharides (LPS) were used to stimulate osteoclast precursor cell RAW264.7 to establish an inflammatory microenvironment and detect osteoclast differentiation. By silencing Btk, the expression of Btk, PLCγ2, and NFATc-1 was detected by real-time qPCR and Western blot, and osteoclastogenesis was detected by enzyme histochemical staining to further confirm the role of Btk in bone resorption. It was found that the expression of Btk, PLCγ2, and NFATc-1 changed significantly with the progression of inflammation and bone destruction, indicating that Btk and PLCγ2 may be involved in the progression of inflammation in apical periodontitis and bone absorption. In vitro experiments confirmed that the differentiation of osteoclasts and the expression of PLCγ2 and NFATc-1 were significantly inhibited after silencing Btk expression, but osteoclast precursor cells could be differentiated due to the proinflammatory factor lipopolysaccharide. This study demonstrates that Btk and PLCγ2 are key factors involved in the apical inflammatory response and bone destruction.

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“…Immunohistochemical staining was carried out in accordance with the methods described in a previous study (Wang et al, ). Briefly, paraffin‐wax slices were dewaxed with gradient alcohol and incubated with 3% H2O2 for 10 min to inactivate endogenous peroxidase, and goat serum blocking solution was used to block the samples for 40 min.…”

Section: Methodsmentioning

confidence: 99%

“…The experiment involved three groups: LTA group, LTA + AG490 group, and the control group. After 24 hr of cell culture, 10 μM JAK2 inhibitor AG490 + 10 μg/ml LTA or 10 μg/ml LTA (Wang et al, ) was used to stimulate cells. The expression of JAK2, p‐JAK2, STAT3, p‐STAT3, and TRAP proteins was detected after 2 and 12 hr of stimulation.…”

Section: Methodsmentioning

confidence: 99%

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JAK2‐STAT3 signaling pathway is involved in rat periapical lesions induced by Enterococcus faecalis

Wang

Jin

et al. 2019

Oral Diseases

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Objectives This study aimed to investigate the role of JAK2‐STAT3 (Janus kinase 2/signal transducer and activator of transcription 3) in periapical disease caused by Enterococcus faecalis, as well as the correlation between lipoteichoic acid (LTA) in E. faecalis and the activity of the JAK2‐STAT3 signaling pathway and osteoclast formation. Materials and Methods A rat model of periapical periodontitis induced by E. faecalis was established. Periapical bone resorption was confirmed by HE staining. The expression of JAK2, p‐JAK2, STAT3, and p‐STAT3 was assessed with immunohistochemical staining. Osteoclasts were observed through enzyme histochemical staining. LTA acted on mouse osteoclast precursor cells (RAW264.7 cells); a JAK2 inhibitor (AG490) was used to inhibit the JAK2‐STAT3 pathway in RAW264.7 cells. The expression of proteins in the JAK2‐STAT3 pathway and TRAP (tartrate resistant acid phosphatase) in RAW264.7 cells was also detected. Results Rat periapical periodontitis was successfully established and bone resorption peaked at day 21. The expression of critical components in the JAK2‐STAT3 pathway increased with the progression of inflammation. LTA promoted the differentiation of RAW264.7 cells into osteoclasts. NFATc1 was highly expressed and was inhibited by AG490. Conclusions JAK2‐STAT3 signaling pathway plays an important role in the process of periapical bone resorption and osteoclastogenesis.

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Enterococcus faecalis Lipoteichoic Acid–induced NLRP3 Inflammasome via the Activation of the Nuclear Factor Kappa B Pathway

Cited by 34 publications

References 35 publications

Sodium Phenylbutyrate Ameliorates Inflammatory Response Induced by Staphylococcus aureus Lipoteichoic Acid via Suppressing TLR2/NF-κB/NLRP3 Pathways in MAC-T Cells

Sodium Phenylbutyrate Ameliorates Inflammatory Response Induced by Staphylococcus aureus Lipoteichoic Acid via Suppressing TLR2/NF-κB/NLRP3 Pathways in MAC-T Cells

Role of the Btk-PLCγ2 Signaling Pathway in the Bone Destruction of Apical Periodontitis

JAK2‐STAT3 signaling pathway is involved in rat periapical lesions induced by Enterococcus faecalis

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