Activation of the NLRP3/caspase-1 inflammasome in human dental pulp tissue and human dental pulp fibroblasts

Jiang, Wenkai; Lv, Haipeng; Wang, Haijing; Wang, Diya; Sun, Shiren; Jia, Qiong; Wang, Peina; Song, Bing; Ni, Longxing

doi:10.1007/s00441-015-2118-7

Cited by 62 publications

(67 citation statements)

References 45 publications

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“…One microgram of total RNA was used as a template to synthesise first-strand complementary DNA using oligo-dT priming with the Omniscript RT kit (Qiagen, USA). QPCR were performed with SYBR Green PCR master mix reagent (Takara, Japan) in an ABI Prism 7500 qPCR system (Advanced Biosystems, USA) as previously described3. The human gene-specific primers for cDNA can be found in Table 1.…”

Section: Methodsmentioning

confidence: 99%

“…Pulpitis is an inflammatory disease which occurs when the infection of caries-related microorganisms penetrates the dentinal tubules and into the pulpal tissue2. During the inflammatory phase, the pulp tissue reacts to bacterial irritants via innate and/or adaptive immune responses, thus releasing a range of chemokines and pro-inflammatory cytokines3. Inflammation and regeneration in dental pulp tissue can appear to be contradictory processes, however, they are clearly inter-related4.…”

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confidence: 99%

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IFN-γ regulates human dental pulp stem cells behavior via NF-κB and MAPK signaling

Jiang

Luo

et al. 2017

Sci Rep

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During caries, dental pulp expresses a range of pro-inflammatory cytokines in response to the infectious challenge. Interferon gamma (IFN-γ) is a dimerized soluble cytokine, which is critical for immune responses. Previous study has demonstrated that IFN-γ at relative high concentration (100 ng/mL) treatment improved the impaired dentinogenic and immunosuppressive regulatory functions of disease-derived dental pulp stem cells (DPSCs). However, little is known about the regulatory effects of IFN-γ at relative low concentration on healthy DPSC behavior (including proliferation, migration, and multiple-potential differentiation). Here we demonstrate that IFN-γ at relatively low concentrations (0.5 ng/mL) promoted the proliferation and migration of DPSCs, but abrogated odonto/osteogenic differentiation. Additionally, we identified that NF-κB and MAPK signaling pathways are both involved in the process of IFN-γ-regulated odonto/osteogenic differentiation of DPSCs. DPSCs treated with IFN-γ and supplemented with pyrrolidine dithiocarbamate (PDTC, an NF-κB inhibitor) or SB203580 (a MAPK inhibitor) showed significantly improved potential for odonto/osteogenic differentiation of DPSCs both in vivo and in vitro. These data provide important insight into the regulatory effects of IFN-γ on the biological behavior of DPSCs and indicate a promising therapeutic strategy for dentin/pulp tissue engineering in future endodontic treatment.

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Section: Methodsmentioning

confidence: 99%

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confidence: 99%

IFN-γ regulates human dental pulp stem cells behavior via NF-κB and MAPK signaling

Jiang

Luo

et al. 2017

Sci Rep

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“…On the other hand, recent studies revealed the importance of the TLR-inflammasome axis in pulpal and periapical inflammatory response [171, 172]. Although macrophage-derived IL-1 is the central mediator in the development of periapical lesions [72, 141], an increased number of NALP3 positive cells, including an influx of myeloids, was quite apparent with the progression of periapical inflammation[172].…”

Section: Non-alcoholic Fatty Liver Disease (Nafld) and Periapical mentioning

confidence: 99%

Interrelationship Between Periapical Lesion and Systemic Metabolic Disorders

Sasaki¹,

Hirai²,

Martins³

et al. 2016

CPD

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Periapical periodontitis, also known as periapical lesion, is a common dental disease, along with periodontitis (gum disease). Periapical periodontitis is a chronic inflammatory disease, caused by endodontic infection, and its development is regulated by the host immune/inflammatory response. Metabolic disorders, which are largely dependent on life style such as eating habits, have been interpreted as a “metabolically-triggered” low-grade systemic inflammation and may interact with periapical periodontitis by triggering immune modulation. The host immune system is therefore considered the common fundamental mechanism of both disease conditions. An elevated inflammatory state caused by metabolic disorders can impact the clinical outcome of periapical lesions and interfere with wound healing after endodontic treatment. Although additional well-designed clinical studies are needed, periapical lesions appear to affect insulin sensitivity and exacerbate non-alcoholic steatohepatitis. Immune regulatory cytokines produced by various cell types, including immune cells and adipose tissue, play an important role in this interrelationship.

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“…Belonging to the Nod-like receptor family, NLRP3 has emerged as the most versatile innate immune receptor because of its broad specificity. 18 Several studies have reported that a broad array of stimuli can activate the NLRP3-CASP1 inflammasome pathway and release of the proinflammatory factor IL1B in immune cells, which is involved in innate immune responses. However, whether Mn, a naturally occurring heavy metal, is involved in the innate immune response through the NLRP3-CASP1 inflammasome pathway in the microglia has yet to be determined.…”

Section: Introductionmentioning

confidence: 99%

The role of NLRP3-CASP1 in inflammasome-mediated neuroinflammation and autophagy dysfunction in manganese-induced, hippocampal-dependent impairment of learning and memory ability

et al. 2017

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Central nervous system (CNS) inflammation and autophagy dysfunction are known to be involved in the pathology of neurodegenerative diseases. Manganese (Mn), a neurotoxic metal, has the potential to induce microglia-mediated neuroinflammation as well as autophagy dysfunction. NLRP3 (NLR family, pyrin domain containing 3)-CASP1 (caspase 1) inflammasome-mediated neuroinflammation in microglia has specific relevance to neurological diseases. However, the mechanism driving these phenomena remains poorly understood. We demonstrate that Mn activates the NLRP3-CASP1 inflammasome pathway in the hippocampus of mice and BV2 cells by triggering autophagy-lysosomal dysfunction. The autophagylysosomal dysfunction is induced by lysosomal damage caused by excessive Mn accumulation, damaging the structure and normal function of these organelles. Additionally, we show that the release of lysosomal CTSB (cathepsin B) plays an important role in Mn-induced NLRP3-CASP1 inflammasome activation, and that the increased autophagosomes in the cytoplasm are not the main cause of NLRP3-CASP1 inflammasome activation. The accumulation of proinflammatory cytokines, such as IL1B (interleukin 1 b) and IL18 (interleukin 18), as well as the dysfunctional autophagy pathway may damage hippocampal neuronal cells, thus leading to hippocampal-dependent impairment in learning and memory, which is associated with the pathogenesis of Alzheimer disease (AD).

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Activation of the NLRP3/caspase-1 inflammasome in human dental pulp tissue and human dental pulp fibroblasts

Cited by 62 publications

References 45 publications

IFN-γ regulates human dental pulp stem cells behavior via NF-κB and MAPK signaling

IFN-γ regulates human dental pulp stem cells behavior via NF-κB and MAPK signaling

Interrelationship Between Periapical Lesion and Systemic Metabolic Disorders

The role of NLRP3-CASP1 in inflammasome-mediated neuroinflammation and autophagy dysfunction in manganese-induced, hippocampal-dependent impairment of learning and memory ability

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