Database : MEDLINE
Search on : Endotoxemia [Words]
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[PMID]: 29240916
[Au] Autor:Hu Y; Li B; Wen L; He K
[Ad] Address:Institute of Veterinary Medicine, Jiangsu Academy of Agricultural Sciences, Nanjing, China.
[Ti] Title:Study on the anti-endotoxin effect of sinomenine using an Agilent genome array.
[So] Source:QJM;111(3):171-178, 2018 Mar 01.
[Is] ISSN:1460-2393
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Background: Endotoxin is a significant contributing factor underlying the occurrence of fever, diarrhea, inflammation, edema, coagulation, shock and other syndromes associated with gram-negative bacterial infections. To date, there is no effective treatment for endotoxemia. Aim: The aim of this study was to characterize differentially expressed genes in sinomenine-treated and lipopolysaccharide (LPS)-induced endothelial cells by microarray analysis and to determine the potential pharmacological activity of sinomenine. Design: The cultured cells of five treatment groups (n = 3) were collected. Participants: total RNA was extracted and subjected to Agilent Porcine 4 × 44 K whole genome microarray. Methods: Kyoto encyclopedia of genes and genomes and gene ontology software were applied to screen and analyze differentially regulated genes. Results: The results showed that 723 differentially regulated genes were identified including 410 up-regulated genes and 313 down-regulated genes in therapy group vs. LPS group. Ten genes may be key controlled genes in the pathogenesis of LPS, including five up-regulated genes (ARG1, TLR2, IL1A, VCAM1, DKK3) and five down-regulated genes (HABP2, ID1, CHDH, GPX3, PTGFR), which primarily contribute to biological processes such as inflammatory response, vascular lesion, metabolic process and cell cycle. IL1A and FMO3 were considered as potent target genes. Conclusion: Global gene expression profile analysis showed that sinomenine might effectively be useful to regulate inflammatory responses as part of future anti-endotoxin therapies.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Process
[do] DOI:10.1093/qjmed/hcx234

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[PMID]: 29417380
[Au] Autor:Towner RA; Saunders D; Smith N; Towler W; Cruz M; Do S; Maher JE; Whitaker K; Lerner M; Morton KA
[Ad] Address:Advanced Magnetic Resonance Center, Oklahoma Medical Research Foundation, 825 N.E. 13th Street, Oklahoma City, OK, 73104, USA. Rheal-Towner@omrf.org.
[Ti] Title:Assessing long-term neuroinflammatory responses to encephalopathy using MRI approaches in a rat endotoxemia model.
[So] Source:Geroscience;40(1):49-60, 2018 02.
[Is] ISSN:2509-2723
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:Sepsis-associated encephalopathy (SAE) induces neuroinflammation, which is associated with cognitive impairment (CI). CI is also correlated with aging. We used contrast-enhanced magnetic resonance imaging (MRI), perfusion MRI, and MR spectroscopy to assess long-term alterations in BBB permeability, microvascularity, and metabolism, respectively, in a rat lipopolysaccharide-induced SAE model. Free radical-targeted molecular MRI was used to detect brain radical levels at 24 h and 1 week post-LPS injection. CE-MRI showed increased Gd-DTPA uptake in LPS rat brains at 24 h in cerebral cortex, hippocampus, thalamus, and perirhinal cortex regions. Increased MRI signal intensities were observed in LPS rat brains in cerebral cortex, perirhinal cortex, and hippocampus regions 1 week post-LPS. Long-term BBB dysfunction was detected in the cerebral cortex at 6 weeks post-LPS. Increased relative cerebral blood flow (rCBF) in cortex and thalamus regions at 24 h, decreased cortical and hippocampal rCBF at 6 weeks, decreased cortical rCBF at 3 and 12 weeks, and increased thalamus rCBF at 6 weeks post-LPS, were detected. MRS indicated that LPS-exposed rat brains had decreased: NAA/Cho metabolite ratios at 1, 3, 6, and 12 weeks; Cr/Cho at 1, 3, and 12 weeks; and Myo-Ins/Cho at 1, 3, and 6 weeks post-LPS. Free radical imaging detected increased radical levels in LPS rat brains at 24 h and 1 week post-LPS. LPS-exposed rats were compared to saline-treated controls. We clearly demonstrated BBB dysfunction, impaired vascularity, and decreased brain metabolites, as measures of long-term neuroinflammatory indicators, as well as increased free radicals in a LPS-induced rat SAE model.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Entry month:1802
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Process
[do] DOI:10.1007/s11357-018-0009-z

  3 / 8149 MEDLINE  
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[PMID]: 29500907
[Au] Autor:Bajaj JS; Kakiyama G; Cox IJ; Nittono H; Takei H; White M; Fagan A; Gavis EA; Heuman DM; Gilles HC; Hylemon P; Taylor-Robinson SD; Legido-Quigley C; Kim M; Xu J; Williams R; Sikaroodi M; Pandak WM; Gillevet PM
[Ad] Address:Virginia Commonwealth University and McGuire Veterans Affairs Medical Center, Richmond, VA, USA.
[Ti] Title:Alterations in Gut Microbial Function Following Liver Transplant.
[So] Source:Liver Transpl;, 2018 Mar 03.
[Is] ISSN:1527-6473
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Liver transplant (LT) improves daily function and ameliorates gut microbial composition. However, the effect of LT on microbial functionality, which can be related to overall patient benefit, is unclear and could affect the post-LT course. AIMS: To determine the effect of LT on gut microbial functionality focusing on endotoxemia, bile acid (BA), ammonia metabolism and lipidomics. METHOD: We enrolled outpatient cirrhotic patients on the LT list and followed them till 6 months post-LT. Microbiota composition (Shannon diversity and individual taxa) and function analysis (serum endotoxin, urinary metabolomics and serum lipidomics, and stool BA profile) and cognitive tests were performed at both visits. RESULTS: We enrolled 40 patients (56±7 years, MELD 23). They received LT 6±3 months after enrollment and were re-evaluated 7±3 months post-LT with a stable course. A significant improvement in cognition with increase in microbial diversity, increase in autochthonous and decrease in potentially pathogenic taxa and reduced endotoxemia were seen post-LT compared to baseline. Stool BAs increased significantly post-LT and there was evidence of greater bacterial action (higher secondary, oxo and iso-BAs) post-LT although the levels of conjugated BAs remained similar. There was a reduced serum ammonia and corresponding rise in urinary phenylacetylglutamine (PAG) post-LT. There was an increase in urinary trimethylamine-N-oxide (TMAO), which was correlated with specific changes in serum lipids related to cell membrane products. The ultimate post-LT lipidomic profile appeared beneficial compared to the pre-LT. CONCLUSIONS: LT improves gut microbiota diversity and dysbiosis which is accompanied by favorable changes in gut microbial functionality corresponding to bile acids, ammonia, endotoxemia, lipidomic and metabolomic profiles. This article is protected by copyright. All rights reserved.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180303
[Lr] Last revision date:180303
[St] Status:Publisher
[do] DOI:10.1002/lt.25046

  4 / 8149 MEDLINE  
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[PMID]: 29420166
[Au] Autor:Ghosh SS; He H; Wang J; Gehr TW; Ghosh S
[Ad] Address:a Department of Internal Medicine , Virginia Commonwealth University Medical Center , Richmond , VA.
[Ti] Title:Curcumin-mediated regulation of intestinal barrier function: The mechanism underlying its beneficial effects.
[So] Source:Tissue Barriers;6(1):e1425085, 2018 Jan 02.
[Is] ISSN:2168-8370
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Curcumin has anti-inflammatory, anti-oxidant and anti-proliferative properties established largely by in vitro studies. Accordingly, oral administration of curcumin beneficially modulates many diseases including diabetes, fatty-liver disease, atherosclerosis, arthritis, cancer and neurological disorders such as depression, Alzheimer's or Parkinson's disease. However, limited bioavailability and inability to detect curcumin in circulation or target tissues has hindered the validation of a causal role. We established curcumin-mediated decrease in the release of gut bacteria-derived lipopolysaccharide (LPS) into circulation by maintaining the integrity of the intestinal barrier function as the mechanism underlying the attenuation of metabolic diseases (diabetes, atherosclerosis, kidney disease) by curcumin supplementation precluding the need for curcumin absorption. In view of the causative role of circulating LPS and resulting chronic inflammation in the development of diseases listed above, this review summarizes the mechanism by which curcumin affects the several layers of the intestinal barrier and, despite negligible absorption, can beneficially modulate these diseases.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180302
[Lr] Last revision date:180302
[St] Status:In-Data-Review
[do] DOI:10.1080/21688370.2018.1425085

  5 / 8149 MEDLINE  
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[PMID]: 29408694
[Au] Autor:Jensen T; Abdelmalek MF; Sullivan S; Nadeau KJ; Green M; Roncal C; Nakagawa T; Kuwabara M; Sato Y; Kang DH; Tolan DR; Sanchez-Lozada LG; Rosen HR; Lanaspa MA; Diehl AM; Johnson RJ
[Ad] Address:Department of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, United States. Electronic address: Thomas.Jensen@ucdenver.edu.
[Ti] Title:Fructose and sugar: A major mediator of non-alcoholic fatty liver disease.
[So] Source:J Hepatol;, 2018 Feb 02.
[Is] ISSN:1600-0641
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome; its rising prevalence parallels the rise in obesity and diabetes. Historically thought to result from overnutrition and a sedentary lifestyle, recent evidence suggests that diets high in sugar (from sucrose and/or high-fructose corn syrup [HFCS]) not only increase the risk of NAFLD, but also non-alcoholic steatohepatitis (NASH). Herein, we review the experimental and clinical evidence that fructose precipitates fat accumulation in the liver, due to both increased lipogenesis and impaired fat oxidation. Recent evidence suggests that the predisposition to fatty liver is linked to the metabolism of fructose by fructokinase C, which results in ATP consumption, nucleotide turnover and uric acid generation that mediate fat accumulation. Alterations to gut permeability, the microbiome, and associated endotoxemia contribute to the risk of NAFLD and NASH. Early clinical studies suggest that reducing sugary beverages and total fructose intake, especially from added sugars, may have a significant benefit on reducing hepatic fat accumulation. We suggest larger, more definitive trials to determine if lowering sugar/HFCS intake, and/or blocking uric acid generation, may help reduce NAFLD and its downstream complications of cirrhosis and chronic liver disease.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1802
[Cu] Class update date: 180302
[Lr] Last revision date:180302
[St] Status:Publisher

  6 / 8149 MEDLINE  
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[PMID]: 29310086
[Au] Autor:Tinkov AA; Gritsenko VA; Skalnaya MG; Cherkasov SV; Aaseth J; Skalny AV
[Ad] Address:Yaroslavl State University, Sovetskaya St., 14, Yaroslavl 150000, Russia; Peoples' Friendship University of Russia (RUDN University), Miklukho-Maklay St., 10/2, Moscow 117198, Russia; Institute of Cellular and Intracellular Symbiosis, Russian Academy of Sciences, Orenburg, 460008, Russia. Electronic
[Ti] Title:Gut as a target for cadmium toxicity.
[So] Source:Environ Pollut;235:429-434, 2018 Apr.
[Is] ISSN:1873-6424
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The primary objective of the present study was to review the impact of Cd exposure on gut microbiota and intestinal physiology, as well as to estimate whether gut may be considered as the target for Cd toxicity. The review is based on literature search in available databases. The existing data demonstrate that the impact of Cd on gut physiology is two-sided. First, Cd exposure induces a significant alteration of bacterial populations and their relative abundance in gut (increased Bacteroidetes-to-Firmicutes ratio), accompanied by increased lipopolysaccharide (LPS) production, reflecting changed metabolic activity of the intestinal microbiome. Second, in intestinal wall Cd exposure induces inflammatory response and cell damage including disruption of tight junctions, ultimately leading to increased gut permeability. Together with increased LPS production, impaired barrier function causes endotoxinemia and systemic inflammation. Hypothetically, Cd-induced increase gut permeability may also result in increased bacterial translocation. On the one hand, bacteriolysis may be associated with aggravation of endotoxemia. At the same time, together with Cd-induced impairment of macrophage inflammatory response, increased bacterial translocation may result in increased susceptibility to infections. Such a supposition is generally in agreement with the finding of higher susceptibility of Cd-exposed mice to infections. The changed microbiome metabolic activity and LPS-induced systemic inflammation may have a significant impact on target organs. The efficiency of probiotics in at least partial prevention of the local (intestinal) and systemic toxic effects of cadmium confirms the role of altered gut physiology in Cd toxicity. Therefore, probiotic treatment may be considered as the one of the strategies for prevention of Cd toxicity in parallel with chelation, antioxidant, and anti-inflammatory therapy.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1801
[Cu] Class update date: 180302
[Lr] Last revision date:180302
[St] Status:In-Process

  7 / 8149 MEDLINE  
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[PMID]: 29490098
[Au] Autor:Aydemir TB; Cousins RJ
[Ad] Address:Food Science and Human Nutrition Department and Center for Nutritional Sciences, College of Agricultural and Life Sciences, University of Florida, Gainesville, FL.
[Ti] Title:The Multiple Faces of the Metal Transporter ZIP14 (SLC39A14).
[So] Source:J Nutr;148(2):174-184, 2018 Feb 01.
[Is] ISSN:1541-6100
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The SLC39A family of metal transporters was identified through homologies with the Zrt- and Irt-like (ZIP) proteins from yeast and plants. Of all the ZIP transporters, ZIP14 is arguably the most robustly characterized in terms of function at the integrative level. Mice with a global knockout of Zip14 are viable, thus providing the opportunity to conduct physiologic experiments. In mice, Zip14 expression is highly tissue specific, with the greatest abundance in the jejunum > liver > heart > kidney > white adipose tissue > skeletal muscle > spleen > pancreas. A unique feature of Zip14 is its upregulation by proinflammatory conditions, particularly increased interleukin 6 (IL-6) and nitric oxide. The transcription factors AP-1, ATF4, and ATF6α are involved in Zip14 regulation. ZIP14 does not appear to be zinc-regulated. The Zip14 knockout phenotype shows multiple sites of ZIP14 function, including the liver, adipose tissue, brain, pancreas, and bone. A prominent feature of the Zip14 ablation is a reduction in intestinal barrier function and onset of metabolic endotoxemia. Many aspects of the phenotype are accentuated with age and accompany increased circulating IL-6. Studies with 65Zn, 59Fe [nontransferrin-bound iron (NTBI)] and 54Mn show that ZIP14 transports these metals. At a steady state, the plasma concentrations of zinc, NTBI, and manganese are such that zinc ions are the major substrate available for ZIP14 at the cell surface. Upregulation of ZIP14 accounts for the hypozincemia and hepatic zinc accumulation associated with acute inflammation and sepsis and is required for liver regeneration and resistance to endoplasmic reticulum (ER) stress. Zip14 ablation in mice produces a defect in manganese excretion that leads to excess manganese accumulation in the brain that produces characteristics of Parkinsonism.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180228
[Lr] Last revision date:180228
[St] Status:In-Data-Review
[do] DOI:10.1093/jn/nxx041

  8 / 8149 MEDLINE  
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[PMID]: 29458051
[Au] Autor:Karthikeyan A; Mohan P; Chinnakali P; Vairappan B
[Ad] Address:Department of Biochemistry, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Pondicherry 605006, India.
[Ti] Title:Elevated systemic zonula occludens 1 is positively correlated with inflammation in cirrhosis.
[So] Source:Clin Chim Acta;480:193-198, 2018 Feb 16.
[Is] ISSN:1873-3492
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND/AIM: It has been well established that disruption of the intestinal barrier function and increased intestinal permeability contribute to endotoxemia and associated liver injury in patients with cirrhosis. However, the relationship between systemic inflammation and tight junction protein in cirrhosis remain unidentified. The aim of this study was to assess and compare the blood concentrations of ZO-1 with systemic hsCRP in patients with cirrhosis and healthy individuals. METHODS: 30 cirrhotic patients and 30 healthy individuals were enrolled in the study. Blood ZO-1 and hsCRP were measured by ELISA and biochemical parameters by AU680 Beckman Coulter (USA) autoanalyser. RESULTS: The serum ALT, AST, bilirubin, gamma GT, ALP and ammonia were significantly (P < 0.0001) elevated whilst serum albumin concentration was decreased in cirrhotic patients when compared to healthy individuals. Systemic tight junction protein ZO-1 concentration [590.0 ±â€¯32.79 vs. 349.9 ±â€¯18.76 pg/ml, respectively; P < 0.0001] and hsCRP [10.50 ±â€¯1.05 vs 5.31 ±â€¯0.65 mg/L, respectively; P < 0.001] were significantly elevated in patients with cirrhosis compared to controls. Significant positive correlation was found between increased ZO-1 and hsCRP (r = 0.2680 P < 0.01). CONCLUSION: Our results suggested that increased systemic ZO-1 concentration was associated with inflammation in cirrhosis. Thus, elevated blood ZO-1 levels could be a prognostic marker of cirrhotic patients with intestinal TJ disruption on the background of inflammation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180228
[Lr] Last revision date:180228
[St] Status:Publisher

  9 / 8149 MEDLINE  
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[PMID]: 29222967
[Au] Autor:Shah FA; Singamsetty S; Guo L; Chuan BW; McDonald S; Cooper BA; O'Donnell BJ; Stefanovski D; Wice B; Zhang Y; O'Donnell CP; McVerry BJ
[Ad] Address:Division of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh, Pittsburgh, Pa. Electronic address: shahfa@upmc.edu.
[Ti] Title:Stimulation of the endogenous incretin glucose-dependent insulinotropic peptide by enteral dextrose improves glucose homeostasis and inflammation in murine endotoxemia.
[So] Source:Transl Res;193:1-12, 2018 Mar.
[Is] ISSN:1878-1810
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Loss of glucose homeostasis during sepsis is associated with increased organ dysfunction and higher mortality. Novel therapeutic strategies to promote euglycemia in sepsis are needed. We have previously shown that early low-level intravenous (IV) dextrose suppresses pancreatic insulin secretion and induces insulin resistance in septic mice, resulting in profound hyperglycemia and worsened systemic inflammation. In this study, we hypothesized that administration of low-level dextrose via the enteral route would stimulate intestinal incretin hormone production, potentiate insulin secretion in a glucose-dependent manner, and thereby improve glycemic control in the acute phase of sepsis. We administered IV or enteral dextrose to 10-week-old male C57BL/6J mice exposed to bacterial endotoxin and measured incretin hormone release, glucose disposal, and proinflammatory cytokine production. Compared with IV administration, enteral dextrose increased circulating levels of the incretin hormone glucose-dependent insulinotropic peptide (GIP) associated with increased insulin release and insulin sensitivity, improved mean arterial pressure, and decreased proinflammatory cytokines in endotoxemic mice. Exogenous GIP rescued glucose metabolism, improved blood pressure, and increased insulin release in endotoxemic mice receiving IV dextrose, whereas pharmacologic inhibition of GIP signaling abrogated the beneficial effects of enteral dextrose. Thus, stimulation of endogenous GIP secretion by early enteral dextrose maintains glucose homeostasis and attenuates the systemic inflammatory response in endotoxemic mice and may provide a therapeutic target for improving glycemic control and clinical outcomes in patients with sepsis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[St] Status:In-Data-Review

  10 / 8149 MEDLINE  
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[PMID]: 29183872
[Au] Autor:Tremellen K; McPhee N; Pearce K; Benson S; Schedlowski M; Engler H
[Ad] Address:Department of Obstetrics Gynaecology and Reproductive Medicine, Flinders University , Bedford Park, South Australia , Australia.
[Ti] Title:Endotoxin-initiated inflammation reduces testosterone production in men of reproductive age.
[So] Source:Am J Physiol Endocrinol Metab;314(3):E206-E213, 2018 Mar 01.
[Is] ISSN:1522-1555
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Inflammation, both acute and chronic, is associated with testosterone deficiency, raising the possibility of a direct causal link. One potential trigger for inflammation in obese men is the passage of intestinal bacteria into the circulation due to a breakdown in mucosal barrier integrity. Recently, we hypothesized that this endotoxin exposure may cause androgen deficiency in obese men. To test this hypothesis, we analyzed the relationship between serum levels of lipopolysaccharide-binding protein (LBP), an indirect measure of endotoxin exposure, against male reproductive hormones, inflammatory markers (C-reactive protein, IL-1ß, IL-6, TNF-α), and adiposity in 75 men. Adiposity was positively correlated with endotoxin exposure (LBP) and inflammation (C-reactive protein, IL-6) and negatively correlated with testosterone. Furthermore, endotoxemia (LBP) was negatively correlated with serum testosterone but positively correlated with IL-6. Multivariate analysis revealed a significant, negative correlation between serum IL-6 and free testosterone. In a second interventional study, low-dose endotoxin challenge in lean men produced a transient inflammatory response that was followed by a decline in serum testosterone, without changes in LH or FSH, providing further evidence that endotoxin-driven inflammation may result in impaired Leydig cell function.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[St] Status:In-Data-Review
[do] DOI:10.1152/ajpendo.00279.2017


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