scholarly journals Sitagliptin Attenuates Porphyromonas Gingivalis Virulence and Inflammatory Response in Macrophage on Titanium

2021 ◽  
Author(s):  
Weilong Tang ◽  
Minquan Du ◽  
Shuang Zhang ◽  
Han Jiang
Keyword(s):  
Inflammatory Response ◽  
Porphyromonas Gingivalis ◽  
Virulence Factors ◽  
Flow Cytometry Assay ◽  
Related Factors ◽  
Qrt Pcr ◽  
Inhibiting Effect ◽  
Porphyromonas Gingivalis Lipopolysaccharide ◽  
Anti Inflammatory ◽  
Inflammatory Effect

Abstract BackgroundIn peri-implantitis, porphyromonas gingivalis and macrophage play central roles. The aim of this study was to detect the attenuating effect of an anti-diabetic drug sitagliptin on porphyromonas gingivalis virulence and inflammatory response in macrophage on titanium discs. Materials and methodsPorphyromonas gingivalis and macrophage were cultured on titanium discs. Antibacterial and antibiofilm activities of sitagliptin were assessed and the morphology of porphyromonas gingivalis were observed by SEM. Bacterial early adhesion, aggregation, hemagglutination, hemolysis and porphyromonas gingivalis virulence factors mRNA expression were assessed to preliminarily investigate the mechanisms of action. Flow cytometry assay, qRT-PCR and Western Blot were used to assess the anti-inflammatory effect of sitagliptin on porphyromonas gingivalis lipopolysaccharide-stimulated macrophage. ResultsThe present study demonstrated the inhibiting effect of sitagliptin on the growth, biofilm, phenotypic behavior and virulence factors of porphyromonas gingivalis and the protective effect on the porphyromonas gingivalis lipopolysaccharide-induced polarization in macrophage. And we also confirmed the anti-inflammatory effect of sitagliptin on the secretion of inflammation-related factors in macrophage by inhibiting the MAPK and AKT signaling pathways. ConclusionsSitagliptin possesses the attenuating effect on porphyromonas gingivalis virulence and inflammatory response in porphyromonas gingivalis lipopolysaccharide-stimulated macrophage on titanium.

scholarly journals Anti-Inflammatory Effect of Ecklonia cava Extract on Porphyromonas gingivalis Lipopolysaccharide-Stimulated Macrophages and a Periodontitis Rat Model

Nutrients ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 1143 ◽  
Author(s):  
Seonyoung Kim ◽  
Soo-Im Choi ◽  
Gun-Hee Kim ◽  
Jee-Young Imm
Keyword(s):  
Porphyromonas Gingivalis ◽  
Nuclear Factor Κb ◽  
Ecklonia Cava ◽  
Heme Oxygenase 1 ◽  
Therapeutic Effects ◽  
Related Factor ◽  
Nuclear Factor ◽  
Porphyromonas Gingivalis Lipopolysaccharide ◽  
Anti Inflammatory ◽  
Inflammatory Effect

Ecklonia cava, an edible marine brown alga (Laminariaceae), is a rich source of phlorotannins. This study aimed to investigate the anti-inflammatory effect of Ecklonia cava ethanol extract (ECE, dieckol 10.6%, w/w) on Porphyromonas gingivalis lipopolysaccharide-stimulated inflammation in RAW 264.7 cells and in ligature-induced periodontitis in rats. The levels of nitric oxide (NO) and prostaglandin E2 were decreased by more than half on treatment with 100 μg/mL ECE. Downregulated tumor necrosis factor-α, interleukin (IL)-1β, and IL-6 gene expression confirmed the anti-inflammatory properties of ECE. ECE treatment upregulated heme oxygenase-1 (HO-1) expression by 6.3-fold and increased HO-1/nuclear factor erythroid 2-related factor 2 (Nrf-2) signaling decreased nuclear factor-κB (NF-κB) translocation. ECE administration (400 mg/kg) significantly reduced gingival index, restricted tooth mobility, and prevented alveolar bone loss (p < 0.05). These beneficial effects were due to decreased inflammatory cell infiltration, IL-1β production, and matrix metalloproteinase expression in gingival tissues. The ratio of receptor activator of nuclear factor-κB ligand (RANKL)/osteoprotegerin, a biomarker of periodontitis and osteolysis, was significantly decreased by ECE administration (p < 0.05). Thus, ECE has potential therapeutic effects for the alleviation of periodontal disease.

Carbon Monoxide-Neuroglobin Axis Targeting Metabolism Against Neuroinflammation

2021 ◽  
Author(s):  
Daniela Dias-Pedroso ◽  
José S. Ramalho ◽  
Vilma A. Sardão ◽  
John G. Jones ◽  
Carlos C. Romão ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Carbon Monoxide ◽  
Oxygen Consumption ◽  
Inflammatory Response ◽  
Microglial Cell ◽  
Cell Metabolism ◽  
Competent Cell ◽  
Metabolic Shift ◽  
Anti Inflammatory ◽  
Inflammatory Effect

Abstract Microglia are the immune competent cell of the central nervous system (CNS), promoting brain homeostasis and regulating inflammatory response against infection and injury. Chronic or exacerbated neuroinflammation is a cause of damage in several brain pathologies. Endogenous carbon monoxide (CO), produced from the degradation of heme, is described as anti-apoptotic and anti-inflammatory in several contexts, including in the CNS. Neuroglobin (Ngb) is a haemoglobin-homologous protein, which upregulation triggers antioxidant defence and prevents neuronal apoptosis. Thus, we hypothesized a crosstalk between CO and Ngb, in particular, that the anti-neuroinflammatory role of CO in microglia depends on Ngb. A novel CO-releasing molecule (ALF826) based on molybdenum was used for delivering CO in microglial culture.BV-2 mouse microglial cell line was challenged with lipopolysaccharide (LPS) for triggering inflammation, and after 6h ALF826 was added. CO exposure limited inflammation by decreasing inducible nitric oxide synthase (iNOS) expression and the production of nitric oxide (NO) and tumour necrosis factor-a (TNF-a), and by increasing interleukine-10 (IL-10) release. CO-induced Ngb upregulation correlated in time with CO’s anti-inflammatory effect. Moreover, knocking down Ngb reversed the anti-inflammatory effect of CO, suggesting that dependents on Ngb expression. CO-induced Ngb upregulation was independent on ROS signalling, but partially dependent on the transcriptional factor SP1. Finally, microglial cell metabolism is also involved in the inflammatory response. In fact, LPS treatment decreased oxygen consumption in microglia, indicating a switch to glycolysis, which is associated with a proinflammatory. While CO treatment increased oxygen consumption, reverting LPS effect and indicating a metabolic shift into a more oxidative metabolism. Moreover, in the absence of Ngb this phenotype was no longer observed, indicating Ngb is needed for CO’s modulation of microglial metabolism. Finally, the metabolic shift induced by CO did not depend on alteration of mitochondrial population. In conclusion, neuroglobin emerges for the first time as a key player for CO signalling against exacerbated neuroinflammation in microglia.

Abstract WP284: Pro-inflammatory Response Elicited by Porphyromonas Gingivalis Lipopolysaccharide Exacerbates the Rupture of Experimental Cerebral Aneurysms

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Takeshi Miyamoto ◽  
Keiko T Kitazato ◽  
Yoshiteru Tada ◽  
Kenji Shimada ◽  
Kenji Yagi ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Porphyromonas Gingivalis ◽  
Intracranial Aneurysms ◽  
Renal Hypertension ◽  
Saline Control ◽  
High Morbidity ◽  
Aneurysmal Rupture ◽  
Porphyromonas Gingivalis Lipopolysaccharide ◽  
Group 2 ◽  
Group 1

Introduction: Subarachnoid hemorrhage (SAH) is a catastrophic event with high morbidity and a poor prognosis. To prevent SAH, its pathogenesis must be understood. Dental infection may play a part in the pathophysiology of intracranial aneurysms. In our newly established rat model of aneurysms, the vascular inflammatory response was associated with their rupture. Therefore we hypothesized that the inflammatory response exacerbated by periodontal pathogens affects experimental cerebral aneurysm rupture. Methods: Aneurysms were induced in 10-week-old female Sprague-Dawley rats by eliciting estrogen deficiency, renal hypertension, and hemodynamic stress. Two weeks later they were divided into 2 groups; group 1 (n=13) was treated with Porphyromonas gingivalis lipopolysaccharide (LPS), group 2 (n=17) was the saline control. Both groups were intraperitoneally injected once a week. Results: During the 90-day observation period, 7 group 1 (54%) and 6 group 2 rats (35%) suffered aneurysmal rupture. The incidence of rupture within 60 days was significantly higher in group 1 than group 2 (38% vs 6%, p<0.05), indicating that LPS promoted experimental aneurysmal rupture. The administration of LPS increased the plasma level of IL-1β and MMP-9 and the mRNA level of TLR2, IL-1β, and MMP-9 in the vascular wall prone to rupture on day 60. In our in vitro studies, IL-1β mRNA was increased in vascular smooth muscle cells exposed to LPS. These results suggest that LPS enhances the rupture of intracranial aneurysms via the promotion of local and systemic pro-inflammatory responses. Conclusion: Our study first documents that in rats, Porphyromonas gingivalis LPS exacerbates vascular inflammation and enhances the rupture of intracranial aneurysms.

scholarly journals Obesity Affects β2 Adrenergic Regulation of the Inflammatory Profile and Phenotype of Circulating Monocytes from Exercised Animals

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2630 ◽  
Author(s):  
Isabel Gálvez ◽  
Leticia Martín-Cordero ◽  
María Dolores Hinchado ◽  
Alberto Álvarez-Barrientos ◽  
Eduardo Ortega
Keyword(s):  
Inflammatory Response ◽  
Adrenergic Receptor ◽  
Acute Exercise ◽  
Inflammatory Responses ◽  
Adrenergic Regulation ◽  
Immune Stress ◽  
Β2 Adrenergic Receptor ◽  
Anti Inflammatory ◽  
Inflammatory Profile ◽  
Inflammatory Effect

Anomalous immune/inflammatory responses in obesity take place along with alterations in the neuroendocrine responses and dysregulation in the immune/stress feedback mechanisms. Exercise is a potential anti-inflammatory strategy in this context, but the influence of exercise on the β2 adrenergic regulation of the monocyte-mediated inflammatory response in obesity remains completely unknown. The first objective of this study was to analyze the effect of exercise on the inflammatory profile and phenotype of monocytes from obese and lean animals, and the second aim was to determine whether obesity could affect monocytes’ inflammatory response to β2 adrenergic activation in exercised animals. C57BL/6J mice were allocated to different lean or obese groups: sedentary, with acute exercise, or with regular exercise. The inflammatory profile and phenotype of their circulating monocytes were evaluated by flow cytometry in the presence or absence of the selective β2 adrenergic receptor agonist terbutaline. Exercise caused an anti-inflammatory effect in obese individuals and a pro-inflammatory effect in lean individuals. β2 adrenergic receptor stimulation exerted a global pro-inflammatory effect in monocytes from exercised obese animals and an anti-inflammatory effect in monocytes from exercised lean animals. Thus, β2 adrenergic regulation of inflammation in monocytes from exercised animals seems to depend on the inflammatory basal set-point.

scholarly journals Anti-inflammatory effect of tricin isolated from Alopecurus aequalis Sobol. on the LPS-induced inflammatory response in RAW 264.7 cells

2016 ◽  
Vol 38 (5) ◽  
pp. 1614-1620 ◽  
Author(s):  
Byoung-Man Kang ◽  
Byoung-Kwan An ◽  
Won-Seok Jung ◽  
Ho-Kyung Jung ◽  
Jung-Hee Cho ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Raw 264.7 Cells ◽  
Raw 264.7 ◽  
Anti Inflammatory ◽  
Inflammatory Effect
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