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1.
Hyperferritinemia in critically ill COVID-19 patients - Is ferritin the product of inflammation or a pathogenic mediator?
Gómez-Pastora, J, Weigand, M, Kim, J, Wu, X, Strayer, J, Palmer, AF, Zborowski, M, Yazer, M, Chalmers, JJ
Clinica chimica acta; international journal of clinical chemistry. 2020;:249-251
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2.
Efficacy of Nutritional Interventions on Inflammatory Markers in Haemodialysis Patients: A Systematic Review and Limited Meta-Analysis.
Khor, BH, Narayanan, SS, Sahathevan, S, Gafor, AHA, Daud, ZAM, Khosla, P, Sabatino, A, Fiaccadori, E, Chinna, K, Karupaiah, T
Nutrients. 2018;(4)
Abstract
Low-grade chronic inflammation is prevalent in patients undergoing haemodialysis (HD) treatment and is linked to the development of premature atherosclerosis and mortality. The non-pharmacological approach to treat inflammation in HD patients through nutritional intervention is well cited. We aimed to assess the efficacy of different nutritional interventions at improving inflammatory outcomes in HD patients, based on markers such as C-reactive protein (CRP), interleukin-6 (IL-6), and tumour necrosis factor-α (TNF-α). We searched PubMed, Cochrane Library, and Embase for randomized controlled trials (RCT) published before June 2017. Inclusion criteria included RCTs on adult patients on maintenance HD treatment with duration of nutritional interventions for a minimum 4 weeks. Risk of bias was assessed using the Jadad score. In total, 46 RCTs experimenting different nutritional interventions were included in the review and categorized into polyphenols rich foods, omega-3 fatty acids, antioxidants, vitamin D, fibres, and probiotics. Meta-analyses indicated significant reduction in CRP levels by omega-3 fatty acids (Random model effect: -0.667 mg/L, p < 0.001) and vitamin E (fixed model effect: -0.257 mg/L, p = 0.005). Evidence for other groups of nutritional interventions was inconclusive. In conclusion, our meta-analysis provided evidence that omega-3 fatty acids and vitamin E could improve inflammatory outcomes in HD patients.
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3.
Local and Systemic Expression of Immunomodulatory Factors in Chronic Pancreatitis.
Komar, HM, Hart, PA, Cruz-Monserrate, Z, Conwell, DL, Lesinski, GB
Pancreas. 2017;(8):986-993
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Abstract
Inflammatory and fibrotic events that drive chronic pancreatitis (CP) are likely orchestrated via signaling of soluble cytokines and chemokines systemically and within the pancreas. However, a comprehensive summary of the expression of such factors during CP has not been reported to date. This information is important given continued interest in targeting cytokines that influence CP pathogenesis. Reported data on the expression change of soluble immunomodulatory factors in human CP patients were identified via a literature search using a single search term. Thirty-one articles meeting the prespecified inclusion criteria were identified to generate a compiled data summary. Compiled data demonstrated up-regulation of several factors in the blood or pancreas microenvironment of CP patients. Nine factors were elevated in both compartments, including fractalkine, IFN-γ, interleukin 1β, IL-6, IL-8, macrophage inhibitory cytokine 1, neutrophil gelatinase-associated lipocalin, transforming growth factor β, and tumor necrosis factor α. Most up-regulated factors could be classified into one of several functional groups, including inflammation, chemotaxis, angiogenesis, bone remodeling, extracellular matrix remodeling, and pain. After further validation, these factors may be used as biomarkers for disease diagnosis and identification of comorbidities, or as potential therapeutic targets.
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Inflammatory biomarkers of coronary heart disease.
Li, H, Sun, K, Zhao, R, Hu, J, Hao, Z, Wang, F, Lu, Y, Liu, F, Zhang, Y
Frontiers in bioscience (Landmark edition). 2017;(3):504-515
Abstract
Coronary heart disease (CHD), characterized by inflammation and accumulation of plaques mainly comprised of lipids, calcium and inflammatory cells in the walls of coronary arteries. CHD is exacerbated by specific cardiovascular risk factors, such as obesity, diabetes mellitus, and hypertension. The current review focuses on the critical role of traditional inflammatory biomarkers, including interleukin-6, C-reactive protein (CRP), complement, CD40 and myeloperoxidase (MPO), in the pathogenesis of CHD.
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Update of syncytiotrophoblast derived extracellular vesicles in normal pregnancy and preeclampsia.
Tannetta, D, Masliukaite, I, Vatish, M, Redman, C, Sargent, I
Journal of reproductive immunology. 2017;:98-106
Abstract
The release of extracellular vesicles (EV) by the syncytiotrophoblast (STB) may be an important mechanism by which the placenta signals to the mother. STB derived EV (STBEV) are comprised predominantly of exosomes (50-150nm) and microvesicles (100-1000nm) that contain bioactive mediators such as proteins, nucleic acids and lipids. They, along with larger syncytial nuclear aggregates are released by the STB into the maternal circulation throughout gestation in normal pregnancy where they appear to have an immunoregulatory role, inhibiting T cell and NK cell responses. In pre-eclampsia (PE) STBEV are released in significantly increased numbers and have pro-inflammatory, anti-angiogenic and procoagulant activity, implicating them in the maternal systemic inflammation, endothelial dysfunction and activation of the clotting system which typifies the disorder. Research has focused on understanding the biological significance of STBEV by measuring their size and repertoire of molecules carried and how they differ in normal pregnancy and PE, using techniques such as Nanoparticle Tracking Analysis, flow cytometry and mass spectrometry. We have also found alterations in STBEV surface glycans associated with PE. The goal is to better understand the role STBEV play in normal pregnancy and PE and whether they are potential biomarkers of placental pathology and therapeutic targets in PE.
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Cardiovascular diseases, depression disorders and potential effects of omega-3 fatty acids.
Trebatická, J, Dukát, A, Ďuračková, Z, Muchová, J
Physiological research. 2017;(3):363-382
Abstract
Cardiovascular disease (CVD) and depressive disorders (DD) are two of the most prevalent health problems in the world. Although CVD and depression have different origin, they share some common pathophysiological characteristics and risk factors, such as the increased production of proinflammatory cytokines, endothelial dysfunction, blood flow abnormalities, decreased glucose metabolism, elevated plasma homocysteine levels, oxidative stress and disorder in vitamin D metabolism. Current findings confirm the common underlying factors for both pathologies, which are related to dramatic dietary changes in the mid-19th century. By changing dietary ratio of omega-6 to omega-3 fatty acids from 1:1 to 15-20:1 some changes in metabolism were induced, such as increased pro-inflammatory mediators and modulations of different signaling pathways following pathophysiological response related to both, cardiovascular diseases and depressive disorders.
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7.
Neuropathology of mood disorders: do we see the stigmata of inflammation?
Mechawar, N, Savitz, J
Translational psychiatry. 2016;(11):e946
Abstract
A proportion of cases with mood disorders have elevated inflammatory markers in the blood that conceivably may result from stress, infection and/or autoimmunity. However, it is not yet clear whether depression is a neuroinflammatory disease. Multiple histopathological and molecular abnormalities have been found postmortem but the etiology of these abnormalities is unknown. Here, we take an immunological perspective of this literature. Increases in activated microglia or perivascular macrophages in suicide victims have been reported in the parenchyma. In contrast, astrocytic markers generally are downregulated in mood disorders. Impairment of astrocytic function likely compromises the reuptake of glutamate potentially leading to excitotoxicity. Inflammatory cytokines and microglia/macrophage-derived quinolinic acid (QA) downregulate the excitatory amino acid transporters responsible for this reuptake, while QA has the additional effect of inhibiting astroglial glutamine synthetase, which converts glutamate to glutamine. Given that oligodendroglia are particularly vulnerable to inflammation, it is noteworthy that reductions in numbers or density of oligodendrocyte cells are one of the most prominent findings in depression. Structural and/or functional changes to GABAergic interneurons also are salient in postmortem brain samples, and may conceivably be related to early inflammatory insults. Although the postmortem data are consistent with a neuroimmune etiology in a subgroup of depressed individuals, we do not argue that all depression-associated abnormalities are reflective of a neuroinflammatory process or even that all immunological activity in the brain is deleterious. Rather, we highlight the pervasive role of immune signaling pathways in brain function and provide an alternative perspective on the current postmortem literature.
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Molecular Imaging of Inflammation: Current Status.
Hammoud, DA
Journal of nuclear medicine : official publication, Society of Nuclear Medicine. 2016;(8):1161-5
Abstract
The ability to image inflammation in vivo can improve our understanding of the pathophysiology underlying various disease etiologies, including cancer, atherosclerosis, and neurodegeneration. A great wealth of preclinical and translational research has been and is currently being developed to decipher the involvement of the immune system in disease pathophysiology, quantify the course of a disease, and visualize the potential detrimental effects of excessive inflammation. Down the road, the ultimate goal is to have clinical noninvasive in vivo imaging biomarkers of inflammation that will help diagnose disease, establish prognosis, and gauge response to preventative and therapeutic strategies.
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9.
Human Milk Components Modulate Toll-Like Receptor-Mediated Inflammation.
He, Y, Lawlor, NT, Newburg, DS
Advances in nutrition (Bethesda, Md.). 2016;(1):102-11
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Abstract
Toll-like receptor (TLR) signaling is central to innate immunity. Aberrant expression of TLRs is found in neonatal inflammatory diseases. Several bioactive components of human milk modulate TLR expression and signaling pathways, including soluble toll-like receptors (sTLRs), soluble cluster of differentiation (sCD) 14, glycoproteins, small peptides, and oligosaccharides. Some milk components, such as sialyl (α2,3) lactose and lacto-N-fucopentaose III, are reported to increase TLR signaling; under some circumstances this might contribute toward immunologic balance. Human milk on the whole is strongly anti-inflammatory, and contains abundant components that depress TLR signaling pathways: sTLR2 and sCD14 inhibit TLR2 signaling; sCD14, lactadherin, lactoferrin, and 2'-fucosyllactose attenuate TLR4 signaling; 3'-galactosyllactose inhibits TLR3 signaling, and β-defensin 2 inhibits TLR7 signaling. Feeding human milk to neonates decreases their risk of sepsis and necrotizing enterocolitis. Thus, the TLR regulatory components found in human milk hold promise as benign oral prophylactic and therapeutic treatments for the many gastrointestinal inflammatory disorders mediated by abnormal TLR signaling.
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Effect of Flaxseed Intervention on Inflammatory Marker C-Reactive Protein: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.
Ren, GY, Chen, CY, Chen, GC, Chen, WG, Pan, A, Pan, CW, Zhang, YH, Qin, LQ, Chen, LH
Nutrients. 2016;(3):136
Abstract
Functional food-flaxseed and its derivatives (flaxseed oil or lignans) are beneficial for human health, possibly because of their anti-inflammatory effects. C-reactive protein (CRP), a sensitive marker of inflammation was chosen to evaluate the anti-inflammatory effects of flaxseed. We searched randomized controlled trials from PubMed and the Cochrane Library in October 2015 and conducted a meta-analysis to evaluate the effectiveness of flaxseed and its derivatives on CRP. The mean differences (net change) in CRP (mg/L) concentrations were pooled with a random- or a fixed-effects model depending on the results of heterogeneity tests. Overall, flaxseed interventions had no effects on reduction of CRP (p = 0.428). The null effects were consistent in the subgroup analysis with multiple studies and population characteristics. Significant heterogeneity was observed in most of the analyses. Meta-regression identified baseline body mass index (BMI) as a significant source of heterogeneity (P-interaction = 0.032), with a significant reduction in CRP of 0.83 mg/L (95% confidence interval -1.34 to -0.31; p = 0.002) among subjects with a BMI of ≥30 kg/m². In conclusion, our meta-analysis did not find sufficient evidence that flaxseed and its derivatives have a beneficial effect on reducing circulating CRP. However, they may significantly reduce CRP in obese populations.