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Porphyromonas gingivalis (Pg) is thought to be involved in the progression of Alzheimer's disease (AD). Whether Pg or its contents can reach the brain and directly affect neuropathology is, however, unknown. Here, we investigated whether outer membrane vesicles (OMVs) of Pg translocate to the brain and induce the pathogenic features of AD.Pg OMVs were injected into the abdominal cavity of mice for 12 weeks. Pg OMV translocation to the brain was detected by immunohistochemistry using an anti-gingipain antibody. Tau protein and microglial activation in the mouse brain were examined by western blotting and immunohistochemistry. The effect of gingipains on inflammation was assessed by real-time polymerase chain reaction using human microglial HMC3 cells.Gingipains were detected in the region around cerebral ventricles, choroid plexus, and ventricular ependymal cells in Pg OMV-administered mice. Tau and phosphorylated Tau protein increased and microglia were activated. Pg OMVs also increased the gene expression of proinflammatory cytokines in HMC3 cells in a gingipain-dependent manner.Pg OMVs, including gingipains, can reach the cerebral ventricle and induce neuroinflammation by activating microglia. Pg OMVs may provide a better understanding of the implications of periodontal diseases in neurodegenerative conditions such as AD.

A new Earth system model of intermediate complexity – CANOPS-GRB v1.0 – is presented for use in quantitatively assessing the dynamics and stability of atmospheric and oceanic chemistry on Earth and Earth-like planets over geologic timescales. The new release is designed to represent the coupled major element cycles of C, N, P, O, and S, as well as the global redox budget (GRB) in Earth's exogenic (ocean–atmosphere–crust) system, using a process-based approach. This framework provides a mechanistic model of the evolution of atmospheric and oceanic O2 levels on geologic timescales and enables comparison with a wide variety of geological records to further constrain the processes driving Earth's oxygenation. A complete detailed description of the resulting Earth system model and its new features are provided. The performance of CANOPS-GRB is then evaluated by comparing a steady-state simulation under present-day conditions with a comprehensive set of oceanic data and existing global estimates of bio-element cycling. The dynamic response of the model is also examined by varying phosphorus availability in the exogenic system. CANOPS-GRB reliably simulates the short- and long-term evolution of the coupled C–N–P–O2–S biogeochemical cycles and is generally applicable across most period of Earth's history given suitable modifications to boundary conditions and forcing regime. The simple and adaptable design of the model also makes it useful to interrogate a wide range of problems related to Earth's oxygenation history and Earth-like exoplanets more broadly. The model source code is available on GitHub and represents a unique community tool for investigating the dynamics and stability of atmospheric and oceanic chemistry on long timescales.

The evolution of land plants in terrestrial environments brought about one of the most dramatic shifts in the history of the Earth system — the birth of modern soils — and likely stimulated massive changes in marine biogeochemistry and climate. In particular, multiple marine mass extinctions characterized by widespread anoxia, including the Late Devonian mass extinction around 375 million years ago (Ma), may have been linked to terrestrial nutrient release driven by newly-rooted landscapes. Here, we use recently generated constraints from Earth’s lacustrine rock record as variable inputs in an Earth system model of the coupled C-N-P-O2-S biogeochemical cycles in order to evaluate whether recorded changes to phosphorus fluxes would be adequate to sustain Devonian marine biogeochemical perturbations and extinction dynamics. Results show that globally scaled riverine phosphorus export during the Late Devonian mass extinction generates widespread marine anoxia and produces carbon isotope, temperature, oxygen, and carbon dioxide perturbations generally consistent with the geologic record. Similar results for a competing extinction mechanism, large scale volcanism, suggest the Late Devonian mass extinction was likely multifaceted with both land plants and volcanism as contributing factors.

Carnosic acid (CA), which is one of bioactive compounds from rosemary, has various biological activities. However, the effect of CA on periodontal ligament cells is still uncertain. The aim of this study was to examine the effects of CA on inflammatory cytokines production in human periodontal ligament cells.Cytokine and chemokine levels were measured by ELISA. Activations of signal transduction pathway were determined by Western blotting.Treatment of CA decreased inflammatory cytokines such as interleukin (IL)-6, CXC chemokine ligand (CXCL)10, CC chemokine ligand (CCL)2, and CCL20 productions in IL-1β or tumor necrosis factor (TNF)-α-stimulated human periodontal ligament cells in a dose-dependent manner. Moreover, we found that CA could suppress Jun-N-terminal kinase (JNK) pathway, nuclear factor (NF)-κB pathway and signal transducer and activator of transcription (STAT)3 pathway activation in IL-1β or TNF-α-stimulated human periodontal ligament cells.The results of this study suggest that CA has anti-inflammatory effects in human periodontal ligament cells by inhibiting JNK, NF-κB and STAT3 pathways.

The global-scale oxygenation of Earth’s surface represents one of the most fundamental chemical transformations in our planet’s history. There is empirical and theoretical evidence for at least two...

Sudachitin, a polymethoxylated flavonoid found in the skin of Citrus sudachi, is a biologically active substance. The aim of this study was to examine whether sudachitin could be used to inhibit the expression of matrix metalloproteinase (MMP)-1 and MMP-3, which are involved in the destruction of periodontal tissues in periodontal lesions, in tumor necrosis factor (TNF)-α-stimulated human periodontal ligament cells (HPDLC). Sudachitin suppressed TNF-α-induced MMP-1 and MMP-3 production in HPDLC. On the other hand, it enhanced tissue inhibitor of metalloproteinase (TIMP)-1 expression. The level of Akt phosphorylation in the TNF-α-stimulated HPDLC was decreased by sudachitin treatment. Moreover, an Akt inhibitor reduced MMP-1 and MMP-3 production and increased TIMP-1 production. These findings indicate that sudachitin reduces MMP-1 and MMP-3 production in TNF-α-stimulated HPDLC by inhibiting the Akt pathway.

Periodontal diseases are common inflammatory diseases that are induced by infection with periodontal bacteria such as Porphyromonas gingivalis (Pg). The association between periodontal diseases and many types of systemic diseases has been demonstrated; the term "periodontal medicine" is used to describe how periodontal infection/inflammation may impact extraoral health. However, the molecular mechanisms by which the factors produced in the oral cavity reach multiple distant organs and impact general health have not been elucidated. Extracellular vesicles (EVs) are nano-sized spherical structures secreted by various types of cells into the tissue microenvironment, and influence pathophysiological conditions by delivering their cargo. However, a detailed understanding of the effect of EVs on periodontal medicine is lacking. In this study, we investigated whether EVs derived from Pg-infected macrophages reach distant organs in mice and influence the pathophysiological status. EVs were isolated from human macrophages, THP-1 cells, infected with Pg. We observed that EVs from Pg-infected THP-1 cells (Pg-inf EVs) contained abundant core histone proteins such as histone H3 and translocated to the lungs, liver, and kidneys of mice. Pg-inf EVs also induced pulmonary injury, including edema, vascular congestion, inflammation, and collagen deposition causing alveoli destruction. The Pg-inf EVs or the recombinant histone H3 activated the NF-κB pathway, leading to increase in the levels of pro-inflammatory cytokines in human lung epithelial A549 cells. Our results suggest a possible mechanism by which EVs produced in periodontal diseases contribute to the progression of periodontal medicine.

The immune response in periodontal lesions is involved in the progression of periodontal disease. Therefore, it is important to find a bioactive substance that has anti-inflammatory effects in periodontal lesions. This study aimed to examine if nobiletin, which is found in the peel of citrus fruits, could inhibit inflammatory responses in interleukin (IL)-1β-stimulated human periodontal ligament cells (HPDLCs). The release of cytokines (IL-6, IL-8, CXCL10, CCL20, and CCL2) and matrix metalloproteinases (MMP-1 and MMP-3) was assessed by ELISA. The expression of cell adhesion molecules (ICAM-1and VCAM-1) and the activation of signal transduction pathways (nuclear factor (NF)-κB, mitogen-activated protein kinases (MAPKs) and protein kinase B (Akt)) in HPDLCs were detected by Western blot analysis.&nbsp, Our experiments revealed that nobiletin decreased the expression of inflammatory cytokines, cell adhesion molecules, and MMPs in IL-1β-stimulated HPDLCs. Moreover, we revealed that nobiletin treatment could suppress the activation of the NF-κB, MAPKs, and Akt pathways. These findings indicate that nobiletin could inhibit inflammatory reactions in IL-1β-stimulated HPDLCs by inhibiting multiple signal transduction pathways, including NF-κB, MAPKs, and Akt.

During the Archean (4.0–2.5 Ga), atmospheric oxygen levels would have been much lower than the present value (pO2 < ~10–5 PAL) [1], and the majority of the primary production would have been carried by anoxygenic photosynthetic bacteria. In a sufficiently reducing atmosphere (CH4/CO2 > ~0.2) [2], the layer of hydrocarbon haze could be formed in the upper atmosphere, possibly affecting the climate. Because haze particles significantly absorb the solar UV flux, the formation of hydrocarbon haze could affect the marine microbial ecosystem via the change in the production rate of electron donors (H2 and CO). However, how the formation of hydrocarbon haze affects the global activity of the marine microbial ecosystem remains unclear. Here, we employ a novel carbon cycle model in which a one-dimensional photochemical model “Atmos” [2], a marine microbial ecosystem model, and the carbonate-silicate geochemical cycle model are coupled. We assessed the effect of the formation of hydrocarbon haze on marine microbial ecosystems assuming completely anoxic conditions (pO2 < ~10–10 PAL) in the middle Archean and assuming mildly oxidized conditions (pO2 > 10–10 PAL) in the late Archean.We found that, under the completely anoxic condition, haze formation works as a negative feedback for the oceanic biological activity. This is because the formation rate of electron donors (H2 and CO) in the atmosphere decreases with the progress of haze formation, so that the changes in the biogenic methane flux and the haze formation rate are suppressed. More specifically, the decrease in the formation rate of electron donors is caused by the decrease in the photo-dissociation rate of CO2 because of UV-shielding due to haze particles, and also by removal of C- and H-atom, which are supposed to be converted to CO and H2 if the haze is not formed, due to rainout of haze particles. We also found that, under the mildly oxidized condition, there are multiple equilibrium climate states that have a different haze thickness. The solution with thicker haze layer is similar to the completely anoxic condition, however, the other solution with the thinner haze layer is unique to the mildly oxidized condition. In this new equilibrium state, the formation rate of electron donors further decreases with the progress of haze formation because of the decrease in the photo-dissociation rate of formaldehyde. Thus, this mechanism works as a strong negative feedback for ocean biological activity and haze thickness, keeping the haze thickness thinner than the completely anoxic condition. We show that, as a result of this negative feedback, climate with the thinner haze could be stably achieved under the mildly oxidized condition. This result is consistent with a geological record which suggests possible transient formation of the haze in the Late Archean [3]. We suggest that haze formation is a vital process in understanding the biological activity and climate stability on terrestrial Earth-like planets.[1] Lyons et al. (2014). Nature 506, 307-315. [2] Arney et al. (2016). Astrobiology 16(11), 873-899. [3] Izon et al. (2017). PNAS 114(13), E2571-E2579.

Earth's modern atmosphere is highly oxygenated and is a remotely detectable signal of its surface biosphere. However, the lifespan of oxygen-based biosignatures in Earth's atmosphere remains uncertain, particularly for the distant future. Here we use a combined biogeochemistry and climate model to examine the likely timescale of oxygen-rich atmospheric conditions on Earth. Using a stochastic approach, we find that the mean future lifespan of Earth's atmosphere with oxygen levels more than 1% of the present atmospheric level is 1.08+-0.14 billion years. The model projects that a deoxygenation of the atmosphere, with atmospheric oxygen dropping sharply to levels reminiscnet of the Archaean Earth, will most probably be triggered before the inception of moist greenhouse conditions in Earth's climate system and before the extensive loss of surface water from the atmosphere. We find that future deoxygenation is an inevitable consequence of increasing solar fluxes, whereas its precise timing is modulated by the exchange flux of reducing power between the mantle and the ocean-atmosphere-crust system. Our results suggest that the planetary carbonate-silicate cycle will tend to lead to terminally CO2-limited biospheres and rapid atmospheric deoxygenation, emphasizing the need for robust atmospheric biosignatures applicable to weakly oxygenated and anoxic exoplanet atmospheres and highlighting the potential importance of atmospheric organic haze during the terminal stages of planetary habitability., Manuscript currently in press in Nature Geoscience

Sudachitin, which is a polymethoxylated flavonoid found in the peel of Citrus sudachi, has some biological activities. However, the effect of sudachitin on periodontal resident cells is still uncertain. The aim of this study was to examine if sudachitin could decrease the expression of inflammatory mediators such as cytokines, chemokines, or matrix metalloproteinase (MMP) in interleukin- (IL-) 1β-stimulated human periodontal ligament cells (HPDLC). Sudachitin inhibited IL-1β-induced IL-6, IL-8, CXC chemokine ligand (CXCL)10, CC chemokine ligand (CCL)2, MMP-1, and MMP-3 production in HPDLC. On the other hand, tissue inhibitor of metalloproteinase- (TIMP-) 1 expression was increased by sudachitin treatment. Moreover, we found that the nuclear factor- (NF-) κB and protein kinase B (Akt) pathways in the IL-1β-stimulated HPDLC were inhibited by sudachitin treatment. These findings indicate that sudachitin is able to reduce inflammatory mediator production in IL-1β-stimulated HPDLC by inhibiting NF-κB and Akt pathways.

Sudachitin, which is a polymethoxylated flavonoid found in the peel of Citrus sudachi, has some biological activities. However, the effect of sudachitin on periodontal resident cells is still uncertain. The aim of this study was to examine if sudachitin could decrease the expression of inflammatory mediators such as cytokines, chemokines, or matrix metalloproteinase (MMP) in interleukin- (IL-) 1β-stimulated human periodontal ligament cells (HPDLC). Sudachitin inhibited IL-1β-induced IL-6, IL-8, CXC chemokine ligand (CXCL)10, CC chemokine ligand (CCL)2, MMP-1, and MMP-3 production in HPDLC. On the other hand, tissue inhibitor of metalloproteinase- (TIMP-) 1 expression was increased by sudachitin treatment. Moreover, we found that the nuclear factor- (NF-) κB and protein kinase B (Akt) pathways in the IL-1β-stimulated HPDLC were inhibited by sudachitin treatment. These findings indicate that sudachitin is able to reduce inflammatory mediator production in IL-1β-stimulated HPDLC by inhibiting NF-κB and Akt pathways.

Earth’s orbital variations on timescales of 104–105 years, known as Milankovitch cycles, have played a critical role in pacing climate change and ecosystem dynamics, through glacial and/or monsoon dynamics. However, the climatic and biotic consequences of these cycles on much longer (~ 107 years) timescales remain unclear, due to a lack of long proxy records with precise age constraints. Here, we show ~ 10-Myr scale variations in early Mesozoic (250–180 Ma) records of lake-level, desert distribution, biogenic-silica burial flux, atmospheric CO2 levels (pCO2), and sea-surface-temperature (SST). Their phase relationships, coupled with carbon cycle modeling results, suggest that orbitally-paced summer monsoon dynamics modulates changes in terrestrial weatherability by ~ 20%, affecting changes in pCO2 of up to 500–1,000 ppmv and 3–7 °C SST. We also infer that these ~ 10-Myr scale climatic variations could have been causally linked to biotic turnover, size variations in dinosaur footprints, and tetrapod dispersal, potentially through spatio-temporal variations in resource availability and arid-hot climatic barriers at low-middle latitudes.

Carnosic acid, which is a bioactive compound isolated from rosemary, has various pharmacological effects. However, the anti-inflammatory effect of carnosic acid on periodontitis is still unknown. The aim of this study was to investigate the effect of carnosic acid on CXC chemokine receptor 3 (CXCR3) ligands, which are involved in Th1 cells migration and accumulation, production in interleukin (IL)-27-stimulated human oral epithelial cells (TR146 cells). Carnosic acid decreased CXC chemokine ligand (CXCL)9, CXCL10, and CXCL11 production in IL-27-stimulated TR146 cells in a dose-dependent fashion. Moreover, we disclosed that carnosic acid could suppress signal transducer and activator of transcription (STAT)1, STAT3, and protein kinase B (Akt) phosphorylation in IL-27-stimulated TR146 cells. Furthermore, STAT1, STAT3, and Akt inhibitors could suppress CXCR3 ligands production in IL-27-treated TR146 cells. In summary, carnosic acid could reduce CXCR3 ligands production in human oral epithelial cell by inhibiting STAT1, STAT3, and Akt activation.

Objectives: The effects of 2-methacryloyloxyethyl phosphorylcholine (MPC)-polymer on the adherence of microorganisms such as non-Candida albicans Candida (NCAC) and methicillin-resistant Staphylococcus aureus (MRSA), frequently detected in oral infections in immunocompromised and/or elderly people, to denture resin material, are still unclear. Here, we report the effects of MPC-polymer on the adherence of C. albicans, NCAC, and MRSA to acrylic denture resin. Methods: Sixteen strains of C. albicans, seven strains of C. glabrata, two strains of C. tropicalis, one strain of C. parapsilosis, and six strains of MRSA were used. We cultured the fungal/bacterial strains and examined the cell growth and adherence of fungi/bacteria to mucin-coated acrylic denture resin plates (ADRP) with or without MPC-polymer coating, by scanning electron microscopy. The cell surface hydrophobicity of the fungal/bacterial strains was measured by the adsorption to hydrocarbons. Results: MPC-polymer did not affect the growth of all strains of Candida species and MRSA, but significantly suppressed adherence to ADRP in most strains of C. albicans and all strains of NCAC and MRSA. A significant positive correlation was found between cell hydrophobicity and the reduction rates of microbial adherence to ADRP treated with 5% of MPC-polymer. Conclusions: MPC-polymer treatment for acrylic resin material suppresses the adherence of C. albicans, NCAC and MRSA via their hydrophilicity interaction. Clinical significance: The application of MPC-polymer for denture hygiene is potent to prevent oral candidiasis, denture stomatitis and opportunistic infection, caused by Candida species and MRSA, via suppressing the adherence of those fungus/bacteria.

Earth's ocean-atmosphere system has undergone a dramatic but protracted increase in oxygen (O2) abundance. This environmental transition ultimately paved the way for the rise of multicellular life and provides a blueprint for how a biosphere can transform a planetary surface. However, estimates of atmospheric oxygen levels for large intervals of Earth's history still vary by orders of magnitude-foremost for Earth's middle history. Historically, estimates of mid-Proterozoic (1.9-0.8 Ga) atmospheric oxygen levels are inferred based on the kinetics of reactions occurring in soils or in the oceans, rather than being directly tracked by atmospheric signatures. Rare oxygen isotope systematics-based on quantifying the rare oxygen isotope 17O in addition to the conventionally determined 16O and 18O-provide a means to track atmospheric isotopic signatures and thus potentially provide more direct estimates of atmospheric oxygen levels through time. Oxygen isotope signatures that deviate strongly from the expected mass-dependent relationship between 16O, 17O, and 18O develop during ozone formation, and these "mass-independent" signals can be transferred to the rock record during oxidation reactions in surface environments that involve atmospheric O2. The magnitude of these signals is dependent upon pO2, pCO2, and the overall extent of biospheric productivity. Here, we use a stochastic approach to invert the mid-Proterozoic Δ17O record for a new estimate of atmospheric pO2, leveraging explicit coupling of pO2 and biospheric productivity in a biogeochemical Earth system model to refine the range of atmospheric pO2 values that is consistent with a given observed Δ17O. Using this approach, we find new evidence that atmospheric oxygen levels were less than ∼1% of the present atmospheric level (PAL) for at least some intervals of the Proterozoic Eon.

Transforming growth factor (TGF)-β1 is a multifunctional cytokine, which can control certain functions of various kinds of cells. However, it is unclear whether TGF-β1 affects T-cell migration in periodontal lesions. The aim of this study was to examine the effects of TGF-β1 on the production of C-C chemokine ligand (CCL)11, which is a T-helper 2-type chemokine, in human periodontal ligament cells (HPDLC). Interleukin (IL)-4 induced CCL11 production, but TGF-β1 did not, in HPDLC. However, TGF-β1 enhanced CCL11 production in IL-4-stimulated HPDLC. Western blot analysis showed that the signal transducer and activator of transcription 6 (STAT6) pathway was highly activated in HPDLC that had been stimulated with both IL-4 and TGF-β1. Mitogen-activated protein kinase activation did not differ between the HPDLC treated with a combination of IL-4 and TGF-β1 and those treated with IL-4 or TGF-β1 alone. Moreover, a STAT6 inhibitor significantly inhibited CCL11 production in HPDLC that had been stimulated with IL-4 and TGF-β1. The current study clearly demonstrated that TGF-β1 enhanced IL-4-induced CCL11 production in HPDLC. The STAT6 pathway is important for CCL11 production in IL-4- and TGF-β1-treated HPDLC.

The evolution of different forms of photosynthetic life has profoundly altered the activity level of the biosphere, radically reshaping the composition of Earth's oceans and atmosphere over time. However, the mechanistic impacts of a primitive photosynthetic biosphere on Earth's early atmospheric chemistry and climate are poorly understood. Here, we use a global redox balance model to explore the biogeochemical and climatological effects of different forms of primitive photosynthesis. We find that a hybrid ecosystem of H2-based and Fe-based anoxygenic photoautotrophs - organisms that perform photosynthesis without producing oxygen - gives rise to a strong nonlinear amplification of Earth's methane (CH4) cycle, and would thus have represented a critical component of Earth's early climate system before the advent of oxygenic photosynthesis. Using a Monte Carlo approach, we find that a hybrid photosynthetic biosphere widens the range of geochemical conditions that allow for warm climate states well beyond either of these metabolic processes acting in isolation. Our results imply that Earth's early climate was governed by a novel and poorly explored set of regulatory feedbacks linking the anoxic biosphere and the coupled H, C and Fe cycles. We suggest that similar processes should be considered when assessing the potential for sustained habitability on Earth-like planets with reducing atmospheres., Comment: Accepted to Nature Geoscience; Final article and Supplementary Information available at https://www.nature.com/articles/s41561-017-0031-2

Background/Aims: Interleukin-27 (IL-27) is a cytokine which belongs to the IL-12 family. However, the role of IL-27 in the pathogenesis of periodontal disease is uncertain. The aim of this study was to examine the effect of IL-27 on chemokine production in TNF-α-stimulated human oral epithelial cells (TR146). Methods: We measured chemokine production in TR146 by ELISA. We used western blot analysis to detect the phosphorylation levels of signal transduction molecules, including STAT1 and STAT3 in TR146. We used inhibitors to examine the role of STAT1 and STAT3 activation. Results: IL-27 increased CXCR3 ligands production in TNF-α-stimulated TR146. Meanwhile, IL-27 suppressed IL-8 and CCL20 production induced by TNF-α. STAT1 phosphorylation level in IL-27 and TNF-α-stimulated TR146 was enhanced in comparison to TNF-α-stimulated TR146. STAT3 phosphorylation level in IL-27-treated TR146 did not change by TNF-α. Both STAT1 inhibitor and STAT3 inhibitor decreased CXCR3 ligands production. STAT1 inhibitor overrode the inhibitory effect of IL-27 on IL-8 and CCL20 production in TNF-α-stimulated TR146. Meanwhile, STAT3 inhibitor did not modulate IL-8 and CCL20 production. Conclusion: IL-27 might control leukocyte migration in periodontal lesion by modulating chemokine production from epithelial cells.

The global silica cycle is an important component of the long-term climate system, yet its controlling factors are largely uncertain due to poorly constrained proxy records. Here we present a ∼70 Myr-long record of early Mesozoic biogenic silica (BSi) flux from radiolarian chert in Japan. Average low-mid-latitude BSi burial flux in the superocean Panthalassa is ∼90% of that of the modern global ocean and relative amplitude varied by ∼20–50% over the 100 kyr to 30 Myr orbital cycles during the early Mesozoic. We hypothesize that BSi in chert was a major sink for oceanic dissolved silica (DSi), with fluctuations proportional to DSi input from chemical weathering on timescales longer than the residence time of DSi (, While the global silica cycle is known to play an important role in long-term climate change, the driving factors remain unknown. Here, the authors present a ∼70 million year long record of early Mesozoic biogenic silica and propose orbitally-paced chemical weathering as a primary driver.

The double-stranded RNA-dependent kinase (PKR), which is activated by double stranded RNA, induces inflammation by regulating NF-κB signaling. The NLR family pyrin domain-containing 3 (NLRP3) inflammasome also modulates inflammation in response to infection. Porphyromonas gingivalis (P.gingivalis) is an oral bacterium which is implicated in the pathogenesis of periodontal diseases. We previously reported that PKR is a key modulator of bone metabolism and inflammation in the periodontal tissue. PKR was also reported to induce inflammation in response to microbes by regulating the NLRP3 inflammasome, suggesting that PKR could affect inflammation along with NLRP3 in periodontal diseases. In this study, we investigated the effects of PKR on NLRP3 expression and NF-κB activity in P. gingivalis infected osteoblasts. We first constructed a SNAP26b-tagged P.gingivalis (SNAP-P. g.) and traced its internalization into the cell. SNAP-P. g. increased the activity of PKR and NF-κB and also induced NLRP3 expression in osteoblasts. Inhibition of NF-κB attenuated SNAP-P. g.-induced NLRP3 expression. The knockdown of PKR using shRNA decreased both the activity of NF-κB and the expression of NLRP3 induced by SNAP-P.g.. We therefore concluded that in osteoblasts, P. gingivalis activated PKR, which in turn increased NLRP3 expression by activating NF-κB. Our results suggest that PKR modulates inflammation by regulating the expression of the NLRP3 inflammasome through the NF-κB pathway in periodontal diseases.