Dysregulation of Inflammasomes in Human Dental Pulp Cells Exposed to Porphyromonas gingivalis and Fusobacterium nucleatum

Aral, Kübra; Milward, Michael; Cooper, Paul R.

doi:10.1016/j.joen.2020.06.008

Cited by 11 publications

(7 citation statements)

References 36 publications

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“…Clarification of the pathways involved in pulpal inflammation is needed to improve treatment strategies in pulpal disease (Aral et al 2020). IL-1b is a major pro-inflammatory cytokine and is involved in pulpal disease (Aral et al 2020). The present study found NLRP6, CASP4, IL1B levels were increased in the inflamed human pulp tissue and both pro-IL-1b and its mature form p17 were detected in the inflamed pulp.…”

Section: Discussionmentioning

confidence: 48%

“…IL‐1β is a major pro‐inflammatory cytokine and is involved in pulpal disease (Aral et al . 2020). The present study found NLRP6 , CASP4 , IL1B levels were increased in the inflamed human pulp tissue and both pro‐IL‐1β and its mature form p17 were detected in the inflamed pulp.…”

Section: Discussionmentioning

confidence: 99%

“…The present study therefore for the first time elucidated the presence and function of NLRP6 inflammasome in HDPCs. Clarification of the pathways involved in pulpal inflammation is needed to improve treatment strategies in pulpal disease (Aral et al 2020). IL-1b is a major pro-inflammatory cytokine and is involved in pulpal disease (Aral et al 2020).…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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NLRP6‐caspase 4 inflammasome activation in response to cariogenic bacterial lipoteichoic acid in human dental pulp inflammation

Tian

Liu

et al. 2021

Int Endodontic J

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Aim To explore the presence and function of NLRP6‐caspase 4 inflammasome in human pulp tissue and human dental pulp cells (HDPCs). Methodology Pulp tissue was collected from freshly extracted human caries‐free third molars and third molars with irreversible pulpitis. Quantitative real‐time polymerase chain reaction (qRT‐PCR) and western blot were performed to assess the expression of NLRP6‐caspase 4 inflammasome. HDPCs were prepared from normal human pulp tissues and challenged with Porphyromonas gingivalis LPS. Enzyme‐linked immunosorbent assay (ELISA) and qRT‐PCR were performed to assess if LPS can upregulate NLRP6 and caspase‐4. HDPCs were further challenged with LPS followed with cytosolic Streptococcus mutans lipoteichoic acid (LTA). SiRNA targeting NLRP6 and Casp4 and pharmacology inhibitor Ac‐FLTD‐CMK and MCC950 were used to assess if Streptococcus mutans LTA can activate the NLRP6 but not the NLRP3 inflammasome. Western blot and ELISA were performed to evaluate inflammasome activation. The Student’s t‐test and one‐way anova were used for statistical analysis. Results NLRP6‐caspase 4 inflammasome was upregulated and activated in inflamed human dental pulp tissue. In HDPCs, Porphyromonas gingivalis LPS upregulated the expression of NLRP6, CASP1 and CASP4 in a type I interferon dependent manner. After LPS priming, cytosolic Streptococcus mutans LTA triggered NLRP6‐caspase 4 inflammasome activation. Knockdown of NLRP6 or CASP4 using siRNA or using pharmacology inhibitor Ac‐FLTD‐CMK but not MCC950 efficiently suppressed inflammasome activation by cytosolic LTA. Conclusions NLRP6‐caspase 4 inflammasome may play an important role in pulp inflammation and immune defence. Inflammatory caspases represent a pharmacological target to restrain pulpal inflammation.

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Section: Discussionmentioning

confidence: 48%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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NLRP6‐caspase 4 inflammasome activation in response to cariogenic bacterial lipoteichoic acid in human dental pulp inflammation

Tian

Liu

et al. 2021

Int Endodontic J

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“…Their products have been shown to induce the expression of AIM2 inflammasomes (Aral, Milward, Gupta, & Cooper, 2020; Ran et al, 2017). Porphyromonas gingivalis , as well as Fusobacterium nucleatum , induces the expression of NLRP3 and AIM2 in macrophages and HDPCs and then results in IL‐1β‐induced pulp inflammation in the presence of ATP (Aral, Milward, & Cooper, 2020; Aral, Milward, Gupta, & Cooper, 2020; Park et al, 2014). Streptococcus mutans can activate the AIM2 inflammasome in macrophage cells (Song et al, 2018).…”

Section: Cytosolic Dna Sensing In Endodontic Infectionmentioning

confidence: 99%

Innate immune sensing of nucleic acid in endodontic infection

et al. 2022

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Innate immunity is the first line of defence and fights against microorganisms.Nucleic acids are important pathogen-associated molecular patterns to be recognized in innate immunity. There are three types of nucleic acid sensors, including endosomal sensors (NA-sensing TLRs), cytosolic DNA sensors (cGAS and AIM2) and cytosolic RNA sensors (RLG-I, MDA5 and LGP2). Recent studies have shown that nucleic acid sensors are expressed differently in a variety of dental pulp cells and mediate inflammation through complex pathways. Nucleic acid sensing may play a vital role in the development of endodontic infection. This review aims to summarize and analyse the possible roles of various nucleic acid sensors in endodontic infection.It may help better understand the pathogenesis of these diseases and find new strategies for prevention and treatment.

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The associations of two novel inflammation indexes, systemic immune-inflammation index (SII) and system inflammation response index (SIRI), with periodontitis: evidence from NHANES 2009–2014

Luo,

Liu,

Jiao

et al. 2024

Clin Oral Invest

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Dysregulation of Inflammasomes in Human Dental Pulp Cells Exposed to Porphyromonas gingivalis and Fusobacterium nucleatum

Cited by 11 publications

References 36 publications

NLRP6‐caspase 4 inflammasome activation in response to cariogenic bacterial lipoteichoic acid in human dental pulp inflammation

NLRP6‐caspase 4 inflammasome activation in response to cariogenic bacterial lipoteichoic acid in human dental pulp inflammation

Innate immune sensing of nucleic acid in endodontic infection

The associations of two novel inflammation indexes, systemic immune-inflammation index (SII) and system inflammation response index (SIRI), with periodontitis: evidence from NHANES 2009–2014

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