Relative abundances of CO2, CO, and CH4 in atmospheres of Earth-like lifeless planets

Carbon is an essential element for life on Earth, and the relative abundances of major carbon species (CO2, CO, and CH4) in the atmosphere exert fundamental controls on planetary climate and biogeochemistry. Here, we employed a theoretical model of atmospheric chemistry to investigate diversity in the atmospheric abundances of CO2, CO, and CH4 on Earth-like lifeless planets orbiting Sun-like (F-, G-, and K-type) stars. We focused on the conditions for the formation of a CO-rich atmosphere, which would be favorable for the origin of life. Results demonstrated that elevated atmospheric CO2 levels trigger photochemical instability of the CO budget in the atmosphere (i.e., CO runaway) owing to enhanced CO2 photolysis relative to H2O photolysis. Higher volcanic outgassing fluxes of reduced C (CO and CH4) also tend to initiate CO runaway. Our systematic examinations revealed that anoxic atmospheres of Earth-like lifeless planets could be classified in the phase space of CH4/CO2 versus CO/CO2, where a distinct gap in atmospheric carbon chemistry is expected to be observed. Our findings indicate that the gap structure is a general feature of Earth-like lifeless planets with reducing atmospheres orbiting Sun-like (F-, G-, and K-type) stars

Nobiletin Decreases Inflammatory Mediator Expression in Tumor Necrosis Factor-Stimulated Human Periodontal Ligament Cells

Nobiletin, a biologically active substance in the skin of citrus fruits, has been reported to be an effective anti-inflammatory, anticancer, and antimicrobial agent. In this study, we aimed to examine the anti-inflammatory effects of nobiletin on tumor necrosis factor- (TNF-) stimulated human periodontal ligament cells (HPDLCs). Our results demonstrated that nobiletin treatment could decrease the expressions of inflammatory cytokines (C-X-C motif chemokine ligand (CXCL)10, C-C motif chemokine ligand (CCL)2, and interleukin- (IL-) 8), matrix metalloproteinases (MMPs) (MMP1 and MMP3), and prostaglandin-endoperoxide synthase 2 (PTGS2) in TNF-stimulated HPDLCs. Moreover, we revealed that nobiletin could inhibit the activation of nuclear factor- (NF-) κB and protein kinase B (AKT1) pathways in TNF-stimulated HPDLCs. Furthermore, nobiletin treatment enhanced nuclear factor, erythroid 2 like 2 (NFE2L2) and heme oxygenase 1 (HMOX1) expressions in TNF-stimulated HPDLCs. In conclusion, these findings suggest that nobiletin can inhibit inflammatory responses in TNF-stimulated HPDLCs by inhibiting NF-κB and AKT1 activations and upregulating the NFE2L2 and HMOX1 expression

TGF-β1 and IL-4 induce CCL11 production

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

Extracellular Vesicles in Periodontal Medicine : The Candidates Linking Oral Health to General Health

The term, periodontal medicine is used to describe the multitude of systemic diseases which are regarded to link periodontal disease. The concept of periodontal medicine has been widely accepted today, however, the molecular mechanisms which periodontal diseases impact general health in whole body are not elucidated in detail. Extracellular vesicles (EVs) and outer membrane vesicles (OMVs) are the nano-sized particles released from mammalian cells and bacterial cells resectively, which influence the health and various disease by transporting biological factors to the neighbor and distant cells. In this review, we will discuss whether EVs and OMVs produced in periodontal diseases could be implicated in periodontal medicine

6-(Methylsulfinyl) Hexyl Isothiocyanate Inhibits IL-6 and CXCL10 Production in TNF-α-Stimulated Human Oral Epithelial Cells

6-(Methylsulfinyl) hexyl isothiocyanate (6-MSITC) is a bioactive substance found in wasabi (Wasabia japonica) and has been reported to have some bioactive effects including anticancer and antioxidant effects. However, there are no reports on its effects on periodontal resident cells, and many points remain unclear. In this study, we aimed to investigate whether 6-MSITC exerts anti-inflammatory effects on human oral epithelial cells, including effects on signal transduction pathway activation. 6-MSITC inhibited interleukin (IL)-6 and C-X-C motif chemokine ligand 10 (CXCL10) production in TNF-α-stimulated TR146 cells, which are a human oral epithelial cell line. Moreover, we found that 6-MSITC could suppress signal transducer and activator of transcription (STAT)3, nuclear factor (NF)-κB, and p70S6 kinase (p70S6K)-S6 ribosomal protein (S6) pathways activation in TNF-α-stimulated TR146 cells. Furthermore, STAT3 and NF-κB inhibitors could suppress IL-6 and CXCL10 production in TNF-α-treated TR146 cells. In summary, 6-MSITC could decrease IL-6 and CXCL10 production in human oral epithelial cell by inhibiting STAT3 and NF-κB activation

Involvement of Fusobacterium Species in Oral Cancer Progression : A Literature Review Including Other Types of Cancer

Chronic inflammation caused by infections has been suggested to be one of the most important cause of cancers. It has recently been shown that there is correlation between intestinal bacteria and cancer development including metastasis. As over 700 bacterial species exist in an oral cavity, it has been concerning that bacterial infection may cause oral cancer. However, the role of bacteria regarding tumorigenesis of oral cancer remains unclear. Several papers have shown that Fusobacterium species deriving the oral cavities, especially, play a crucial role for the development of colorectal and esophageal cancer. F. nucleatum is a well-known oral bacterium involved in formation of typical dental plaque on human teeth and causing periodontal diseases. The greatest characteristic of F. nucleatum is its ability to adhere to various bacteria and host cells. Interestingly, F. nucleatum is frequently detected in oral cancer tissues. Moreover, detection of F. nucleatum is correlated with the clinical stage of oral cancer. Although the detailed mechanism is still unclear, Fusobacterium species have been suggested to be associated with cell adhesion, tumorigenesis, epithelial-to-mesenchymal transition, inflammasomes, cell cycle, etc. in oral cancer. In this review, we introduce the reports focused on the association of Fusobacterium species with cancer development and progression including oral, esophageal, and colon cancers