scholarly journals Systematic review and meta-analysis of the associations of vegan and vegetarian diets with inflammatory biomarkers

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Juliane Menzel ◽  
Afraa Jabakhanji ◽  
Ronald Biemann ◽  
Knut Mai ◽  
Klaus Abraham ◽  
...  
Keyword(s):  
Systematic Review ◽  
Meta Analysis ◽  
Interleukin 1 ◽  
Mean Difference ◽  
Inflammatory Biomarkers ◽  
Vegan Diet ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Necrosis Factor Alpha ◽  
Cross Sectional

AbstractPlant-based diets like vegetarian or vegan diets might influence circulating levels of inflammatory biomarkers, thereby reducing the risk of chronic diseases. This systematic review and meta-analysis aimed to investigate the associations of veganism and vegetarianism with circulating inflammatory biomarkers in comparison to omnivores. Literature search was conducted in Pubmed and EMBASE until April 2020 and mean differences of biomarkers were assessed for: C-reactive protein (CRP), interleukin-6 (IL-6), interleukin-18 (IL-18), interleukin-1 receptor antagonist (IL-1 RA), tumor necrosis factor-alpha (TNF-ɑ), E-selectin, intercellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein-1 (MCP-1), adiponectin, omentin-1 and resistin. Of initially identified 1073 publications, 21 cross-sectional studies met the inclusion criteria and were included in the systematic review and meta-analysis. Vegan diet was associated with lower levels of CRP compared to omnivores [mean difference − 0.54 mg/l, 95%-CI: − 0.79 to − 0.28, p < 0.0001]. This association was less pronounced in vegetarians [mean difference − 0.25 mg/l, 95%-CI: − 0.49 to 0.00, p = 0.05]. In patients with impaired kidney function, the association between vegetarian nutrition and CRP was much stronger with − 3.91 mg/l (95%-CI: − 5.23 to − 2.60; p < 0.0001). No substantial effects were observed for all other inflammatory biomarkers. Despite strong associations between CRP and a vegan or vegetarian diet were seen, further research is needed, as most inflammatory biomarkers were investigated only in single studies so far.

scholarly journals Biochemical Evaluation of the Antioxidant Effects of Hydroxytyrosol on Pancreatitis-Associated Gut Injury

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 781 ◽  
Author(s):  
Roberta Fusco ◽  
Marika Cordaro ◽  
Rosalba Siracusa ◽  
Ramona D’Amico ◽  
Tiziana Genovese ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Interleukin 1 ◽  
Antioxidant Properties ◽  
Pancreatic Tissue ◽  
Intercellular Adhesion Molecule ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Intercellular Adhesion Molecule 1 ◽  
Colon Tissue ◽  
Necrosis Factor Alpha

Acute pancreatitis is a severe abdominal pathology often associated with several complications including gut dysfunction. Oxidative stress is one of the most important pathways involved in this pathology. Hydroxytyrosol (HT), a phenolic compound obtained from olive oil, has shown anti-inflammatory and antioxidant properties. We evaluated the effects of HT administration on pancreatic and intestinal injury induced by caerulein administration. CD1 female mice were administered caerulein (50 μg/kg) for 10 h. HT treatment (5 mg/kg) was performed 30 min after the first caerulein injection and for two consecutive hours afterwards. One hour after the last caerulein injection, mice were sacrificed and serum, colon and pancreatic tissue samples were collected. HT was able to reduce the serum hallmarks of pancreatitis (amylase and lipase), histological damage score in both pancreas and colon tissue, inflammatory cells recruitment (mast cells) in both injured tissues, intrapancreatic trypsin activity and overexpression of the adhesion molecules (Intercellular Adhesion Molecule-1 (ICAM-1) and P-selectin) in colon. Additionally, HT reduced cytokine (interleukin 1 beta (IL- 1β), interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α)) levels in serum, pancreas and colon tissue and chemokine release (monocyte chemotactic protein-1 (MCP1/CCL2)) in pancreas and colon tissue. HT decreased lipid peroxidation and oxidative stress (superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione S-transferase (GST) activity) by enhancing the nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) in both injured tissues. Moreover, HT preserved intestinal barrier integrity, as shown by the diamine oxidase (DAO) serum levels and tight junction (zonula occludens (ZO) and occludin) expression in pancreas and colon. Our findings demonstrated that HT would be an important therapeutic tool against pancreatitis-induced injuries in the pancreas and gut.

scholarly journals Host Inflammatory Biomarkers of Disease Severity in Pediatric Community-Acquired Pneumonia: A Systematic Review and Meta-analysis

2019 ◽  
Vol 6 (12) ◽  
Author(s):  
Catarina D Fernandes ◽  
María B Arriaga ◽  
Maria Carolina M Costa ◽  
Maria Clara M Costa ◽  
Maria Heloina M Costa ◽  
...  
Keyword(s):  
Systematic Review ◽  
Disease Severity ◽  
Clinical Decision Making ◽  
Meta Analysis ◽  
Clinical Decision ◽  
Serum Levels ◽  
Community Acquired Pneumonia ◽  
Inflammatory Biomarkers ◽  
Cross Sectional ◽  
Cell Counts

Abstract Background Community-acquired pneumonia (CAP) is the leading cause of death in children. Identification of reliable biomarkers offers the potential to develop a severity quantitative score to assist in clinical decision-making and improve outcomes. Methods A systematic review and meta-analysis was performed in PubMed and EMBASE on November 13, 2018, to examine the association between host inflammatory biomarkers and CAP severity in children. The inclusion criteria were case–control, cross-sectional, and cohort studies that examined candidate serum biomarkers. We extracted outcomes of interest, means, and standardized mean differences (SMDs) of plasma and serum levels of biomarkers together with information on disease severity. Meta-analysis was performed. This review was registered in the PROSPERO international registry (CRD42019123351). Results Two hundred seventy-two abstracts were identified, and 17 studies were included. Among the biomarkers evaluated, levels of C-reactive protein (CRP; SMD, 0.63; 95% confidence interval [CI], 0.35 to 0.91), interleukin (IL)-6 (SMD, 0.46; 95% CI, 0.25 to 0.66), IL-8 (SMD, 0.72; 95% CI, 0.15 to 1.29), neutrophil count (SMD, 0.27; 95% CI, 0.07 to 0.47), and procalcitonin (SMD, 0.68; 95% CI, 0.20 to 1.15) were substantially increased in severe CAP. In contrast, IL-2 concentrations (SMD, –0.24; 95% CI, –0.45 to –0.03) were higher in nonsevere CAP. Study heterogeneity was reported to be high (I2 &gt; 75%), except for IL-2, IL-5, IL-6, and IL-12p70, which were classified as moderate (I2 = 50%–74%). Only neutrophil and white blood cell counts were described by studies exhibiting a low level of heterogeneity. Conclusions Our results suggest that host biomarkers, and especially CRP, IL-6, IL-8, and procalcitonin levels, have the potential to predict severe CAP in pediatric populations.

Nuclear Factor κB and Anesthetic Preconditioning during Myocardial Ischemia-Reperfusion

2004 ◽  
Vol 100 (3) ◽  
pp. 540-546 ◽  
Author(s):  
Caiyun Zhong ◽  
Yamei Zhou ◽  
Hong Liu
Keyword(s):  
Ischemia Reperfusion ◽  
Interleukin 1 ◽  
Intercellular Adhesion Molecule ◽  
Nuclear Factor ◽  
Intercellular Adhesion Molecule 1 ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Nf Kappab ◽  
Myocardial Ischemia Reperfusion ◽  
Oxide Synthase

Background Volatile anesthetic preconditioning (APC) protects against myocardial ischemia-reperfusion (IR) injury, but the precise mechanisms underlying this phenomenon remain undefined. To investigate the molecular mechanism of APC in myocardial protection, the activation of nuclear factor (NF) kappaB and its regulated inflammatory mediators expression were examined in the current study. Methods Hearts from male rats were isolated, Langendorff perfused, and randomly assigned to one of three groups: (1) the control group: hearts were continuously perfused for 130 min; (2) the IR group: 30 min of equilibration, 15 min of baseline, 25 min of ischemia, 60 min of reperfusion; and (3) the APC + IR group: 30 min of equilibration, 10 min of sevoflurane exposure and a 5-min washout, 25 min of global ischemia, 60 min of reperfusion. Tissue samples were acquired at the end of reperfusion. NF-kappaB activity was determined by electrophoretic mobility shift assay. The NF-kappaB inhibitor, IkappaB-alpha, was determined by Western blot analysis. Myocardial inflammatory mediators, including tumor necrosis factor alpha, interleukin 1, intercellular adhesion molecule 1, and inducible nitric oxide synthase, were also assessed by Western blot analysis. Results Nuclear factor kappaB-DNA binding activity was significantly increased at the end of reperfusion in rat myocardium, and cytosolic IkappaB-alpha was decreased. Supershift assay revealed the involvement of NF-kappaB p65 and p50 subunits. APC with sevoflurane attenuated NF-kappaB activation and reduced the expression of tumor necrosis factor alpha, interleukin 1, intercellular adhesion molecule 1, and inducible nitric oxide synthase. APC also reduced infarct size and creatine kinase release and improved myocardial left ventricular developed pressure during IR. Conclusions The results of this study indicate that attenuation of NF-kappaB activation and subsequent down-regulation of NF-kappaB-dependent inflammatory gene expression plays an important role in the protective mechanism of APC against acute myocardial IR injury.

scholarly journals Age-Dependent Levels of Select Immunological Mediators in Sera of Healthy Children

1998 ◽  
Vol 5 (1) ◽  
pp. 28-32 ◽  
Author(s):  
Ulrich Sack ◽  
Ullrich Burkhardt ◽  
Michael Borte ◽  
Hiltrud Schädlich ◽  
Kerstin Berg ◽  
...  
Keyword(s):  
Interleukin 1 ◽  
Physical Growth ◽  
Intercellular Adhesion Molecule ◽  
Healthy Children ◽  
Intercellular Adhesion Molecule 1 ◽  
Necrosis Factor Alpha ◽  
Age Related ◽  
Tnf Α ◽  
Age Dependent ◽  
Ifn Γ

ABSTRACT Serum cytokine levels were measured in 275 healthy children of different ages (3 to 17 years). Interleukin-1 receptor antagonist (IL-1RA), soluble IL-2R (sIL-2R) (sCD25), IL-6, IL-8, tumor necrosis factor alpha (TNF-α), soluble TNF receptor type II (sTNF-RII) (sCD120b), gamma interferon (IFN-γ), soluble intercellular adhesion molecule 1 (sICAM-1) (sCD54), soluble E selectin (sE-selectin) (ELAM-1; sCD62E), sCD14, and neopterin were measured with commercial test kits. The mean levels of IL-1RA, sIL-2R, TNF-α, sICAM-1, sE-selectin, and sCD14 were higher than in healthy adults. In contrast, IFN-γ and IL-8 were hardly detectable in children and thereby significantly lower than in adults. In the case of TNF-α, sICAM-1, sE selectin, and sCD14, there was a high interindividual variability, apparently unrelated to disease. The profiles of some cytokines, i.e., IL-1RA, IL-6, and TNF-α, showed age-related increases that overlapped with known patterns of physical growth. Of note, sIL-2R and sE-selectin instead declined with time. Because of the remarkable age-dependent variability in healthy pediatric subjects, disease-related changes, as well as therapy-dependent alterations, should be considered with caution.

scholarly journals Monocyte adhesion to cerebromicrovascular endothelial cells derived from hypertensive and normotensive rats

1994 ◽  
Vol 267 (6) ◽  
pp. H2491-H2497 ◽  
Author(s):  
R. M. McCarron ◽  
L. Wang ◽  
A. L. Siren ◽  
M. Spatz ◽  
J. M. Hallenbeck
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Interleukin 1 ◽  
Intercellular Adhesion Molecule ◽  
Monocyte Adhesion ◽  
Blood Monocytes ◽  
Intercellular Adhesion Molecule 1 ◽  
Necrosis Factor Alpha ◽  
Stroke Risk Factor ◽  
Adhesive Interactions

The stroke risk factor hypertension may function as a predisposing agent by increasing the vulnerability of blood vessels to thrombosis or hemorrhage. The research here demonstrates that cerebrovascular endothelial cells (EC) from spontaneously hypertensive (SHR) and Wistar-Kyoto normotensive (WKY) rats exhibit similar levels of adhesiveness for syngeneic peripheral blood monocytes (e.g., 22.53 +/- 1.32 and 24.35 +/- 1.16%, respectively). Monocyte adhesion to SHR EC was dramatically increased by treatment of EC with lipopolysaccharide, interferon-gamma, or interleukin-1 beta and tumor necrosis factor-alpha (e.g., 106, 68, and 171%, respectively). Identical treatment of WKY EC also increased adhesion albeit at significantly lower levels than observed on concomitantly tested SHR EC (e.g., 47.8, 12.7, and 60.7%, respectively). Allogeneic combinations of monocytes and EC again demonstrated significantly more upregulation of adhesion by treatment of SHR EC than WKY EC. Characterization of these adhesive interactions revealed the interplay of adhesion pathways, which include lymphocyte functional antigen-1/intercellular adhesion molecule-1 (ICAM-1), Mac-1/ICAM-1, and very late activation antigen-4/vascular adhesion molecule-1 as well as other undetermined mechanisms. In summary, these findings indicate hypertension may enhance responsiveness of endothelium to factors that promote monocyte adhesion.

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