Porphyromonas gingivalis regulates atherosclerosis through an immune pathway.

Atherosclerosis (AS) is a chronic inflammatory disease, involving a pathological process of endothelial dysfunction, lipid deposition, plaque rupture, and arterial occlusion, and is one of the leading causes of death in the world population. The progression of AS is closely associated with several inflammatory diseases, among which periodontitis has been shown to increase the risk of AS. Porphyromonas gingivalis (P. gingivalis), presenting in large numbers in subgingival plaque biofilms, is the "dominant flora" in periodontitis, and its multiple virulence factors are important in stimulating host immunity. Therefore, it is significant to elucidate the potential mechanism and association between P. gingivalis and AS to prevent and treat AS. By summarizing the existing studies, we found that P. gingivalis promotes the progression of AS through multiple immune pathways. P. gingivalis can escape host immune clearance and, in various forms, circulate with blood and lymph and colonize arterial vessel walls, directly inducing local inflammation in blood vessels. It also induces the production of systemic inflammatory mediators and autoimmune antibodies, disrupts the serum lipid profile, and thus promotes the progression of AS. In this paper, we summarize the recent evidence (including clinical studies and animal studies) on the correlation between P. gingivalis and AS, and describe the specific immune mechanisms by which P. gingivalis promotes AS progression from three aspects (immune escape, blood circulation, and lymphatic circulation), providing new insights into the prevention and treatment of AS by suppressing periodontal pathogenic bacteria.

Direct electrochemistry and electrocatalysis of myoglobin immobilized on Fe2O3 nanoparticle-sodium alginate-ionic liquid composite-modified electrode.

A biocomposite material composed of sodium alginate (SA), Fe(2)O(3) nanoparticles, and ionic liquid 1-decyl-3-methylimidazolium bromide ([DMIM]Br) was fabricated and used for the immobilization of myoglobin (Mb) on the surface of a carbon ionic liquid electrode (CILE). The CILE was fabricated by mixing graphite powder with ionic liquid N-butylpyridinium hexafluorophosphate (BPPF(6)) together. UV-Vis absorption and FTIR spectroscopic results indicated that Mb retained its native structure in the composite material. A pair of well-defined redox peaks appeared on the cyclic voltammogram in pH 7.0 phosphate buffer solution (PBS) with the formal peak potential (E(0')) at -0.256 V (versus SCE), which was the typical electrochemical behavior of Mb heme Fe(III)/Fe(II) redox couples. The Mb-modified electrode showed good electrocatalytic activity to the reduction of trichloroacetic acid (TCA) and NaNO(2) with wide linear range, good sensitivity, and reproducibility. The calibration range for TCA detection was between 0.6 and 12.0 mmol L(-1) with the linear regression equation as Iss (µA)=42.44C (mmol L(-1))+50.57 and a detection limit of 0.4 mmol L(-1) (3σ). The Mb-modified electrode also applied to NaNO(2) determination in the concentration range from 4.0 to 100.0 mmol L(-1) with a detection limit of 1.3 mmol L(-1) (3σ). So the proposed electrode has potential applications as third-generation biosensors.