scholarly journals Bacterial Translocation Associates With Aggression in Schizophrenia Inpatients

2021 ◽  
Vol 15 ◽  
Author(s):  
Chong Wang ◽  
Teng Zhang ◽  
Lei He ◽  
Ji-Yong Fu ◽  
Hong-Xin Deng ◽  
...  
Keyword(s):  
Bacterial Translocation ◽  
Serum Levels ◽  
Leaky Gut ◽  
Soluble Cd14 ◽  
Reactive Protein ◽  
History Of ◽  
Factor Α ◽  
Overt Aggression Scale ◽  
Anti Inflammation ◽  
Necrosis Factor

Objective: Accumulating evidence indicates that inflammation abnormalities may contribute to aggression behaviors in psychotic patients, however, the possible sources of inflammation remain elusive. We aimed to evaluate the associations among aggression, inflammation, and bacterial translocation (BT) in aggression-affected schizophrenia (ScZ) inpatients with 2 weeks of antipsychotics discontinuation.Methods: Serum specimens collected from 112 aggression and 112 non-aggression individuals with ScZ and 56 healthy adults were used for quantifications of inflammation- or BT-related biomarkers. Aggression severity was assessed by Modified Overt Aggression Scale (MOAS).Results: Proinflammation phenotype dominated and leaky gut-induced BT occurred only in cases with ScZ with a history of aggression, and the MOAS score positively related to levels of C-reactive protein, interleukin (IL)-6, IL-1β, and tumor necrosis factor-α. Furthermore, serum levels of BT-derived lipopolysaccharide (LPS), as well as LPS-responded soluble CD14, were not only positively correlated with levels of above proinflammation mediators but also the total MOAS score and subscore for aggression against objects or others.Conclusion: Our results collectively demonstrate the presence of leaky gut and further correlate BT-derived LPS and soluble CD14 to onset or severity of aggression possibly by driving proinflammation response in inpatients with ScZ, which indicates that BT may be a novel anti-inflammation therapeutic target for aggression prophylaxis.

scholarly journals Relationship between smoking and indicators of systemic inflammation in patients with coronary heart disease

2017 ◽  
Vol 95 (3) ◽  
pp. 264-271
Author(s):  
E. D. Bazdyrev ◽  
O. M. Polikutina ◽  
N. A. Kalichenko ◽  
Yu. S. Slepynina ◽  
E. G. Uchasova ◽  
...  
Keyword(s):  
Systemic Inflammation ◽  
Inflammatory Markers ◽  
Reactive Protein ◽  
Tnf Α ◽  
History Of ◽  
Artery Disease ◽  
Factor Α ◽  
Metalloproteinase 9 ◽  
Necrosis Factor ◽  
Nonspecific Inflammation

Aim. To estimate the severity of systemic inflammation in subjects with coronary artery disease (CAD) without bronchopulmonary system comorbidity depending on smoking factor. Materials and methods. The subjects were divided into groups depending on smoking factor. We estimated the following laboratory markers of nonspecific inflammation: interleukine (IL)-12, -1β, tumour necrosis factor-α, matrix metalloproteinase-9, C-reactive protein. The examination of lungs respiratory function included spirometry, body plethysmography and assessment of diffusing lung capacity. Results. 29.9% of the subjects with CAD smoked, 40% reported discontinuation of smoking in their histories. Smoking in CAD subjects without the history of bronchopulmonary system comorbidity was associated with a higher level of inflammatory markers (IL-12, IL-1β, TNF-α, ММР-9 and CRP) than in subjects who ceased to smoke and those who have never smoked. No differences in the levels of inflammatory markers were revealed in subjects who had smoked before and never smoked. Conclusion. Smoking is widespread among CAD subjects. It is associated with a higher level of markers of nonspecific inflammation as compared to subjects who have never smoked before or ceased smoking.

Genetic Variation in TNF-α, its Relation with Inflammatory Biomarkers and Susceptibility to Rheumatoid Arthritis

2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Khadiga Ahmed Ismail
Keyword(s):  
Rheumatoid Arthritis ◽  
Serum Level ◽  
Functional Disability ◽  
Serum Levels ◽  
Amplification Refractory Mutation System ◽  
Reactive Protein ◽  
Tnf Α ◽  
Mutation System ◽  
Potential Factor ◽  
Factor Α

Background: Tumor necrosis Factor-α (TNF-α) is encoded and controlled by TNF-α gene, which is involved in rheumatoid arthritis (RA) susceptibility. This research aimed to identify genetic variations of TNF-α (G308A) and to establish its association with inflammatory markers in Rheumatoid Arthritis predisposition. Methods: In the present study, fifty RA patients and fifty volunteers were involved and evaluated for the C-reactive protein, rheumatoid factor, and TNF-α were estimated by ELISA, Erythrocyte Sedimentation Rate (ESR) by Wintergreen method and for TNF-α-308 G>A polymorphism by polymerase chain reaction with amplification refractory mutation system (PCR-ARMS). Results: The CRP, RF, ESR and TNF-α were significantly elevated in RA patients relative to controls. The serum level TNF-α was also significantly elevated in female patients and in patients ≥50 years. Analysis of TNF-308 gene polymorphism revealed that GG genotypes were more prevalent in RA patients than in the healthy individuals and that GG genotype may be a potential factor to RA. The G allele was more common in RA than in the control. Elevated TNF-α serum levels were significantly associated the GG genotype and functional disability in RA patients. Conclusion: TNF-α promoter 308polymorphism GG genotype may be considered as a risk factor for RA and the TNF-α serum level was significantly related to the functional disability in the disease.

scholarly journals Upregulation of miR-150-5p alleviates LPS-induced inflammatory response and apoptosis of RAW264.7 macrophages by targeting Notch1

2020 ◽  
Vol 15 (1) ◽  
pp. 544-552
Author(s):  
Xiaoyan Deng ◽  
Zhixing Lin ◽  
Chao Zuo ◽  
Yanjie Fu
Keyword(s):  
Inflammatory Response ◽  
Underlying Mechanism ◽  
Notch Receptor ◽  
Raw264.7 Cells ◽  
Luciferase Reporter ◽  
Raw264.7 Macrophages ◽  
Factor Α ◽  
Anti Inflammation ◽  
Necrosis Factor ◽  
Dual Luciferase Reporter Assay

AbstractCirculating miR-150-5p has been identified as a prognostic marker in patients with critical illness and sepsis. Herein, we aimed to further explore the role and underlying mechanism of miR-150-5p in sepsis. Quantitative real-time-PCR assay was performed to detect the expression of miR-150-5p upon stimulation with lipopolysaccharide (LPS) in RAW264.7 cells. The levels of tumor necrosis factor-α, interleukin (IL)-6 and IL-1β were measured by ELISA assay. Cell apoptosis was determined using flow cytometry. Western blot was used to assess notch receptor 1 (Notch1) expression in LPS-induced RAW264.7 cells. Dual-luciferase reporter assay was employed to validate the target of miR-150-5p. Our data showed that miR-150-5p was downregulated and Notch1 was upregulated in LPS-stimulated RAW264.7 cells. miR-150-5p overexpression or Notch1 silencing alleviated LPS-induced inflammatory response and apoptosis in RAW264.7 cells. Moreover, Notch1 was a direct target of miR-150-5p. Notch1 abated miR-150-5p-mediated anti-inflammation and anti-apoptosis in LPS-induced RAW264.7 cells. miR-150-5p alleviated LPS-induced inflammatory response and apoptosis at least partly by targeting Notch1 in RAW264.7 cells, highlighting miR-150-5p as a target in the development of anti-inflammation and anti-apoptosis drugs for sepsis treatment.

C1QTNF6 participates in the pathogenesis of PCOS by affecting the inflammatory response of granulosa cells

2021 ◽  
Author(s):  
Sisi Yan ◽  
Jinli Ding ◽  
Yi Zhang ◽  
Jiayu Wang ◽  
Sainan Zhang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Mouse Models ◽  
Granulosa Cells ◽  
Polycystic Ovary ◽  
Serum Levels ◽  
Inflammatory Factors ◽  
Low Grade ◽  
Reactive Protein ◽  
Reproductive Endocrine ◽  
Factor Α

Abstract Polycystic ovary syndrome (PCOS) is a common reproductive endocrine disease. It has been reported that chronic low-grade inflammation might participate in its pathogenesis. C1q and TNF related 6 (C1QTNF6) is a newly identified adiponectin paralog associated with inflammation. The aim of the present study was to investigate the role of C1QTNF6 in the development of chronic inflammation in PCOS and the underlying molecular mechanism. After analyzing the expression of C1QTNF6 in the serum and granulosa cells (GCs) of PCOS patients and healthy controls, we verified the roles of C1QTNF6 in inflammation through dehydroepiandrosterone-induced PCOS mouse models and cell models of lipopolysaccharide (LPS)-induced inflammation. The results demonstrated that C1QTNF6 expression in the serum and GCs of patients with PCOS was significantly elevated compared with those of the controls, and similar results were observed in the serum and ovary of PCOS mouse models. In PCOS mice and C1QTNF6-overexpressing PCOS mice, serum levels of pro-inflammatory factors including C-reactive protein (CRP), interleukin 6 (IL6) and tumor necrosis factor-α (TNFα) were increased, while the opposite effects were observed when C1QTNF6 was downregulated in PCOS mice. Furthermore, C1QTNF6 overexpression upregulated the levels of TNFα, IL6, and CRP and activated the AKT/NF-κB pathway in LPS-treated KGN cells, whereas C1QTNF6 knockdown and BAY-117082 (an NF-κB inhibitor) treatment resulted in the opposite effects. Taken together, our results indicate that C1QTNF6 is involved in the pathogenesis of PCOS by affecting the inflammatory response via the AKT/NF-κB signaling pathway.

scholarly journals Quality of Dabai Pulp Oil Extracted by Supercritical Carbon Dioxide and Supplementation in Hypercholesterolemic Rat—A New Alternative Fat

Foods ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 262
Author(s):  
Noor Atiqah Aizan Abdul Kadir ◽  
Azrina Azlan ◽  
Faridah Abas ◽  
Intan Safinar Ismail
Keyword(s):  
Fatty Acid Content ◽  
Total Antioxidant Status ◽  
High Cholesterol Diet ◽  
Reactive Protein ◽  
Total Antioxidant ◽  
Canarium Odontophyllum ◽  
Coa Reductase ◽  
Factor Α ◽  
Necrosis Factor

Dabai pulp oil (DPO) is new oil extracted from the pulp of Canarium odontophyllum. The quality and efficacy of DPO are needed to promote its potential as a new alternative fat. Therefore, we investigate the quality of DPO, which includes moisture and volatile content (MVC), free fatty acid content (FFA), iodine value (IV), and peroxide value (PV). Furthermore, we evaluate the efficacy of DPO against hypercholesterolemia elicited by a high-cholesterol diet in rats. The MVC of DPO was <0.001 ± 0.00%. Next, the FFA in DPO was 2.57 ± 0.03%, and the IV of DPO was 53.74 ± 0.08 g iodine/100 g oil. Meanwhile, the PV of DPO was 4.97 ± 0.00 mEq/kg. Supplementation of DPO in hypercholesterolemic rats for 30 days revealed the hypocholesterolemic effect (significant reduction of total cholesterol, triglyceride, and 3-hydroxy-3-methylglutaryl-CoA reductase) accompanied by a significant reduction of inflammatory markers (C-reactive protein, interleukin-6 and tumour necrosis factor-α), and lipid peroxidation (MDA). We also observed a significant improvement of lipoprotein lipase (LPL) and antioxidant capacities (total antioxidant status, superoxide dismutase, glutathione peroxidase, and catalase) of the rats. The results on the quality and efficacy of locally made DPO suggest its potential use as a healthy alternative fat in the future.

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