scholarly journals Lipopolysaccharide-Induced Neutrophil Dysfunction Following Transjugular Intrahepatic Portosystemic Stent Shunt (TIPSS) Insertion is Associated with Organ Failure and Mortality

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Jane Macnaughtan ◽  
Rajeshwar P. Mookerjee ◽  
Schalk van der Merwe ◽  
Rajiv Jalan
Keyword(s):  
Venous Blood ◽  
Alcoholic Cirrhosis ◽  
Neutrophil Function ◽  
Ros Production ◽  
Variceal Haemorrhage ◽  
Functional Defect ◽  
Organ Failures ◽  
Portal Venous Blood ◽  
Reactive Oxidant ◽  
Underlying Mechanisms

Abstract Systemic lipopolysaccharide (LPS) is implicated in increasing mortality in patients with alcoholic hepatitis but the underlying mechanisms are not well characterised. The objective of this study was to characterise neutrophil function, LPS and cytokine concentrations within the splanchnic circulation of alcoholic cirrhotic patients undergoing TIPSS insertion for variceal haemorrhage and correlate this with outcome. 26 patients with alcoholic cirrhosis and variceal haemorrhage were studied prior to and 1-hour after TIPSS insertion. Neutrophil function, LPS and cytokine concentrations were determined in arterial, hepatic venous (HV) and portal venous blood (PV). Significantly higher LPS concentrations and neutrophil reactive oxidant species (ROS) production were observed in PV vs HV blood. Cross-incubation of HV plasma with PV neutrophils resulted in reduced ROS production. Insertion of TIPSS was associated with a significant increase in arterial LPS concentrations and deterioration in neutrophil phagocytosis. Number of organ failures and arterial IL-6 concentrations at presentation were associated with increased mortality. The portal circulation has a distinct immunological milieu characterised by a pathological neutrophil phenotype and an anti-inflammatory cytokine profile associated with heightened LPS levels. TIPSS insertion renders this neutrophil functional defect systemic, associated with an increase in arterial LPS and a susceptibility to sepsis.

Effect of probiotic treatment on deranged neutrophil function and cytokine responses in patients with compensated alcoholic cirrhosis

2008 ◽  
Vol 48 (6) ◽  
pp. 945-951 ◽  
Author(s):  
Vanessa Stadlbauer ◽  
Rajeshwar P. Mookerjee ◽  
Stephen Hodges ◽  
Gavin A.K. Wright ◽  
Nathan A. Davies ◽  
...  
Keyword(s):  
Alcoholic Cirrhosis ◽  
Neutrophil Function ◽  
Cytokine Responses ◽  
Probiotic Treatment

scholarly journals Intestinal Permeability Assays: a Review

2021 ◽  
Vol 31 (1) ◽  
pp. 20-30
Author(s):  
A. A. Iakupova ◽  
S. R. Abdulkhakov ◽  
R. K. Zalyalov ◽  
A. G. Safin ◽  
R. A. Abdulkhakov
Keyword(s):  
Intestinal Permeability ◽  
Ex Vivo ◽  
Venous Blood ◽  
Intestinal Barrier ◽  
Intestinal Lumen ◽  
Alcoholic Fatty Liver ◽  
Key Points ◽  
Assessment Techniques ◽  
Portal Venous Blood

Aim. A literature review of intestinal permeability assessment techniques.Key points. The intestinal barrier is a functional entity separating the intestinal lumen and internal body, and intestinal permeability is a measure of the barrier functionality. The intestinal barrier integrity and permeability assays differ by the application setting (in vivo or ex vivo), subject (human or animal), marker molecules used to assess permeability (ions, various size carbohydrates, macromolecules, antigens, bacterial products and bacteria), biomaterial for the marker concentration assays (peripheral blood, portal venous blood, urine, stool). Despite a great variety of methods for assessing intestinal permeability, their clinical application requires further studies due to a lack of standardisation, the complexity of selected techniques and occasional limited reliability of results.Conclusion. Further investigation and improvement of intestinal permeability assays is required. The assay and result standardisation will facilitate practice in functional and organic intestinal diseases, as well as allergies, diabetes mellitus, non-alcoholic fatty liver disease and some other illnesses.

scholarly journals Activated T Cells and Soluble Molecules in the Portal Venous Blood of Patients with Cholestatic and Hepatitis C Virus-Positive Liver Cirrhosis. Possible Promotion of Fas/FasL-Mediated Apoptosis in the Bile-Duct Cells and Hepatocyte Injury

2003 ◽  
Vol 31 (3) ◽  
pp. 170-180 ◽  
Author(s):  
N Ariki ◽  
Y Morimoto ◽  
T Yagi ◽  
T Oyama ◽  
Y Cyouda ◽  
...  
Keyword(s):  
T Cells ◽  
Liver Cirrhosis ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Bile Duct ◽  
Venous Blood ◽  
Activated T Cells ◽  
Peripheral Venous Blood ◽  
Nk T Cells ◽  
Portal Venous Blood

We investigated the immune responses of patients with cholestatic and hepatitis C virus-positive (HCV-positive) liver cirrhosis by analysing T-cell subsets and cytokine levels in the portal and peripheral veins, using flow cytometry and enzyme-linked immunosorbent assay. In cholestatic liver cirrhosis, the proportion of natural-killer (NK) T cells and interleukin (IL) 6 and IL-18 levels in the portal venous blood were significantly higher than those in the peripheral venous blood. In HCV-positive liver cirrhosis, the proportions of NK T cells and Fas+ T cells and IL-6 and soluble Fas levels in the portal venous blood were significantly higher than those in the peripheral venous blood. These results suggest that in these diseases, activated T cells and soluble molecules in portal venous blood may promote Fas/FasL-mediated apoptosis of the bile-duct cells and hepatocytes, and contribute to the deterioration in liver function as an inevitable result of positive feedback.

Effect of pre-reperfusion portal venous blood flush on early liver transplant function

1996 ◽  
pp. 188-190
Author(s):  
D. F. Mirza ◽  
B. K. Gunson ◽  
H. Khalaf ◽  
J. W. Freeman ◽  
J. A. C. Buckels ◽  
...  
Keyword(s):  
Liver Transplant ◽  
Venous Blood ◽  
Portal Venous Blood ◽  
Transplant Function

Water Absorption From the Intestine via Portal and Lymphatic Pathways

1956 ◽  
Vol 184 (3) ◽  
pp. 441-444 ◽  
Author(s):  
John A. Benson ◽  
Philip R. Lee ◽  
John F. Scholer ◽  
Kwang S. Kim ◽  
Jesse L. Bollman
Keyword(s):  
Small Intestine ◽  
Venous Blood ◽  
The Body ◽  
Sodium Ion ◽  
Arterial Circulation ◽  
Intestinal Lymph ◽  
Arterial Blood ◽  
Portal Venous Blood ◽  
Lymphatic Pathway ◽  
Lymphatic Pathways

The content of either D2O or Na24 has been measured in the intestinal lymph, portal venous blood, and femoral arterial blood of unanesthetized hydrated rats after administration of the isotope into the stomach, duodenum, or peripheral or portal vein. Little, if any, water or sodium ion is delivered to the body by a lymphatic pathway after absorption from the small intestine. At least 99% is carried in portal venous blood. The amount of isotope found in intestinal lymph was proportional to lymph volume whatever the route of administration, and derived mainly from the arterial blood. Even during absorption of water or sodium ion from the small intestine the arterial circulation is the principal source of the water and sodium of the lymph.

scholarly journals Combination Treatment with Cold Physical Plasma and Pulsed Electric Fields Augments ROS Production and Cytotoxicity in Lymphoma

Cancers ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 845 ◽  
Author(s):  
Christina M. Wolff ◽  
Juergen F. Kolb ◽  
Klaus-Dieter Weltmann ◽  
Thomas von Woedtke ◽  
Sander Bekeschus
Keyword(s):  
Electric Fields ◽  
Combination Treatment ◽  
Argon Plasma ◽  
Pulsed Electric Fields ◽  
Drug Uptake ◽  
Minor Role ◽  
Ros Production ◽  
Treatment Regimens ◽  
Underlying Mechanisms ◽  
Physical Plasma

New approaches in oncotherapy rely on the combination of different treatments to enhance the efficacy of established monotherapies. Pulsed electric fields (PEFs) are an established method (electrochemotherapy) for enhancing cellular drug uptake while cold physical plasma is an emerging and promising anticancer technology. This study aimed to combine both technologies to elucidate their cytotoxic potential as well as the underlying mechanisms of the effects observed. An electric field generator (0.9–1.0 kV/cm and 100-μs pulse duration) and an atmospheric pressure argon plasma jet were employed for the treatment of lymphoma cell lines as a model system. PEF but not plasma treatment induced cell membrane permeabilization. Additive cytotoxicity was observed for the metabolic activity and viability of the cells while the sequence of treatment in the combination played only a minor role. Intriguingly, a parallel combination was more effective compared to a 15-min pause between both treatment regimens. A combination effect was also found for lipid peroxidation; however, none could be observed in the cytosolic and mitochondrial reactive oxygen species (ROS) production. The supplementation with either antioxidant, a pan-caspase-inhibitor or a ferroptosis inhibitor, all partially rescued lymphoma cells from terminal cell death, which contributes to the mechanistic understanding of this combination treatment.

Leukotriene B4 promotes reactive oxidant generation and leukocyte adherence during acute hypoxia

2001 ◽  
Vol 91 (3) ◽  
pp. 1160-1167 ◽  
Author(s):  
Dawn R. S. Steiner ◽  
Norberto C. Gonzalez ◽  
John G. Wood
Keyword(s):  
Acute Hypoxia ◽  
Leukotriene B4 ◽  
Ros Generation ◽  
Leukocyte Adherence ◽  
Systemic Hypoxia ◽  
Microvascular Alterations ◽  
Reactive Oxidant ◽  
Underlying Mechanisms ◽  
Mesenteric Microcirculation

Acute systemic hypoxia produces rapid leukocyte adherence in the rat mesenteric microcirculation, although the underlying mechanisms are not fully known. Hypoxia is known to increase reactive oxygen species (ROS) generation, which could result in formation of the lipid inflammatory mediator leukotriene B4 (LTB4). The goal of this study was to examine the role of LTB4 in hypoxia-induced microvascular alterations. Using intravital microscopy, we determined the effect of the LTB4 antagonist, LTB4-dimethyl amide (LTB4-DMA), on ROS generation and leukocyte adherence in mesenteric venules during hypoxia. Exogenous LTB4 increased ROS generation to 144 ± 8% compared with control values and also promoted leukocyte adherence. These responses to LTB4 were blocked by pretreating the mesentery with LTB4-DMA. Leukopenia did not significantly attenuate the LTB4-induced increase in ROS generation (142 ± 12.1%). LTB4-DMA substantially, though not completely, reduced hypoxia-induced ROS generation from 66 ± 18% to 11 ± 4% above control values. Hypoxia-induced leukocyte adherence was significantly attenuated by LTB4-DMA. Our results support a role for LTB4in the mechanism of hypoxia-induced ROS generation and leukocyte adherence in the rat mesenteric microcirculation.

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