Early interactions ofEntamoeba histolyticatrophozoites with parenchymal and inflammatory cells in the hamster liver: an immunocytochemical study

2002 ◽  
Vol 48 (2) ◽  
pp. 123-131 ◽  
Author(s):  
J Ventura-Juárez ◽  
R Campos-Rodríguez ◽  
V Tsutsumi
Keyword(s):  
Endothelial Cells ◽  
Entamoeba Histolytica ◽  
Close Contact ◽  
Inflammatory Cells ◽  
Ultrastructural Level ◽  
Target Cells ◽  
Nonparenchymal Cells ◽  
Hepatic Cells ◽  
Pmn Leukocytes ◽  
Parenchymal Cells

We studied the early in situ interactions of live and fixed Entamoeba histolytica trophozoites with hamster hepatic parenchymal and inflammatory cells using immunoperoxidase and immunoelectronmicroscopy. Close contact between trophozoites and endothelial cells and the diffusion of amoebic molecules from trophozoites towards nearby endothelial cells and distant hepatocytes were observed. The inflammatory cells around the amoebae and the remnants of parenchymal cells and hepatocytes located close to the lesion had a positive stain for amoebic molecules. In the amoebae, at the ultrastructural level, molecules were attached to the membranes and inside the vesicles. These molecules were apparently released into the space formed between the parasite and the endothelial cells. The endothelial cells and the nearby and distant hepatocytes captured amoebic molecules, and later they became necrotic. Contrarily, when fixed amoebae were inoculated, amoebic molecules were captured by endothelial cells and polymorphonuclear (PMN) leukocytes, but neither suffered any damage. In this work, we are presenting evidence clearly showing that some molecules of the amoeba can diffuse away long distances causing cytotoxic effects and even necrosis on hepatic cells of hamster liver without the need of the trophozoite being in close contact with the target cells. They also may promote lytic or proinflammatory effects by inducing the secretion of enzymes or cytokines in other nonparenchymal cells, like PMN leukocytes and endothelial cells. Our results suggest that the accepted mechanisms of cytotoxicity by amoebae are not exclusively restricted to the following sequence: adhesion, phagocytosis, and necrosis.Key words: amoebiasis, Entamoeba histolytica, liver, hamster, immunocytochemistry.

Endotoxin stimulates gene expression of ROS-eliminating pathways in rat hepatic endothelial and Kupffer cells

1996 ◽  
Vol 270 (4) ◽  
pp. G660-G666 ◽  
Author(s):  
Z. Spolarics
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Kupffer Cells ◽  
Glucose Transporter ◽  
Mrna Levels ◽  
Sod Activity ◽  
Bacterial Killing ◽  
Glut 1 ◽  
Hepatic Cells ◽  
Parenchymal Cells

Reactive oxygen species (ROS) are mediators of cellular injury and play a putative role in the onset of hepatic damage during endotoxemia or sepsis. It has been suggested that induction of glucose-6-phosphate (G-6-P) dehydrogenase, the key enzyme of the hexose monophosphate shunt (HMS), may support ROS-producing or ROS-eliminating pathways in hepatic endothelial and Kupffer cells during endotoxemia. The aim of the study was to assess in vivo lipopolysaccharide (LPS)-induced alterations in rat gene expression of selected enzymes that are in functional relationship with the HMS. mRNA levels and activities of glucose transporter GLUT-1, Mn- and CuZn-dependent superoxide dismutases (Mn-SOD and CuZn-SOD), and Se-dependent glutathione peroxidase (Se-GPX) were determined. Cellular extracts were analyzed 7 or 22 h after injection of LPS (Escherichia coli, 2 mg/kg ip) or injection of saline. Exposure to LPS for 7 or 22 h caused a 10- to 25-fold increase in GLUT-1 mRNA levels in endothelial and Kupffer cells. In parenchymal cells, GLUT-1 mRNA expression was low, and LPS caused no marked changes. Cellular levels of Mn-SOD mRNA were 20-40 times greater in all hepatic cells from LPS-treated animals than in cells from control rats. LPS at 22 h increased Mn-SOD activity by 45% in endothelial cells but caused no significant changes in Kupffer or parenchymal cells. Message levels and enzyme activities of CuZn-SOD and Se-GPX were significantly elevated 22 h after LPS injection in endothelial cells only. Thus LPS results in marked upregulation of functionally related genes in hepatic cells. In endothelial cells, the simultaneous upregulation of GLUT-1, G-6-P dehydrogenase, Mn-SOD, CuZn-SOD, and Se-GPX may represent an important mechanism for accelerated elimination of ROS released from activated sinusoidal phagocytes. In Kupffer cells, upregulated GLUT-1 and G-6-P dehydrogenase, together with constitutively present SOD and lack of upregulated Se-GPX, suggest an elevated capacity to produce O2- and H2O2 that is consistent with primed bacterial killing.

scholarly journals Viral Regulation of RANTES Expression during Human Cytomegalovirus Infection of Endothelial Cells

2001 ◽  
Vol 75 (7) ◽  
pp. 3383-3390 ◽  
Author(s):  
Marcella Billstrom Schroeder ◽  
G. Scott Worthen
Keyword(s):  
Endothelial Cells ◽  
Human Cytomegalovirus ◽  
Hcmv Infection ◽  
Mononuclear Cells ◽  
Viral Gene Expression ◽  
Inflammatory Cells ◽  
Viral Gene ◽  
Circulating Cells ◽  
A Site ◽  
Parenchymal Cells

ABSTRACT Human cytomegalovirus (HCMV) evades healthy immune responses during infection, and this evasion may allow HCMV to establish latency in the host. The human vasculature has been recognized as a site of HCMV infection and may also be a site of latent HCMV infection. As the interface between circulating cells and underlying parenchymal cells, the vascular endothelium provides signals for local reaction of inflammatory cells. We propose that HCMV down-regulates expression of the proinflammatory chemokine RANTES from the infected endothelium, which may result in reduced recruitment of mononuclear cells to the site of infection. Abortive HCMV infection of primary endothelial cells with the clinical isolate HCMV 4010, under conditions in which viral gene expression could not occur, induced high levels of RANTES expression. Replicative HCMV infection, however, induced cells in parallel cultures to express significantly lower levels of RANTES. Expression of the chemokines interleukin 8 and MCP-1 by endothelial cells was found to be unaffected by replicative HCMV infection and thus may not play an important role during early HCMV infection of the endothelium. HCMV may regulate RANTES expression from endothelial cells as a mechanism to evade the local immune response to infection.

scholarly journals Liver-Derived Exosomes and Their Implications in Liver Pathobiology

2018 ◽  
Vol 19 (12) ◽  
pp. 3715 ◽  
Author(s):  
Sumi Sung ◽  
Jieun Kim ◽  
Youngmi Jung
Keyword(s):  
Liver Diseases ◽  
The Body ◽  
Target Cells ◽  
Liver Sinusoidal Endothelial Cells ◽  
Nonparenchymal Cells ◽  
Hepatic Cells ◽  
Donor Cells ◽  
Wide Range ◽  
Potential Applications ◽  
Health And Disease

The liver has a wide range of physiological functions in the body, and its health is maintained by complex cross-talk among hepatic cells, including parenchymal hepatocytes and nonparenchymal cells. Exosomes, which are one method of cellular communication, are endosomal-derived small vesicles that are released by donor cells and delivered to the target cells at both short and long distances. Because exosomes carry a variety of cargoes, including proteins, mRNAs, microRNAs and other noncoding RNAs originating from donor cells, exosomes convey cellular information that enables them to potentially serve as biomarkers and therapeutics in liver diseases. Hepatocytes release exosomes to neighboring hepatocytes or nonparenchymal cells to regulate liver regeneration and repair. Nonparenchymal cells, including hepatic stellate cells, liver sinusoidal endothelial cells, and cholangiocytes, also secrete exosomes to regulate liver remodeling upon liver injury. Exosomes that are released from liver cancer cells create a favorable microenvironment for cancer growth and progression. In this review, we summarize and discuss the current findings and understanding of exosome-mediated intercellular communication in the liver, with a particular focus on the function of exosomes in both health and disease. Based on the current findings, we suggest the potential applications of exosomes as biomarkers and therapeutics for liver diseases.

scholarly journals A cell based assay for evaluating binding and uptake of an antibody using hepatic nonparenchymal cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yuki Noguchi ◽  
Kazuhisa Ozeki ◽  
Hiroaki Takesue ◽  
Hidetaka Akita
Keyword(s):  
Flow Cytometry ◽  
Endothelial Cells ◽  
Liver Sinusoidal Endothelial Cells ◽  
Nonparenchymal Cells ◽  
A Cell ◽  
Hepatic Nonparenchymal Cells ◽  
Titration Assay ◽  
Parenchymal Cells

AbstractEvaluation of the binding and uptake of an antibody in liver non-parenchymal cells (NPC), including liver sinusoidal endothelial cells, is important for revealing its pharmacokinetic (PK) behavior, since NPC has important roles in eliminating an antibody from the blood via the Fc fragment of IgG receptor IIB (FcγRIIB). However, there is currently no in vitro quantitative assay using NPC. This study reports on the development of a cell-based assay for evaluating the binding and uptake of such an antibody using liver NPC of mice and monkeys. In mice, the FcγRIIB-expressing cells were identified in the CD146-positive and CD45-negative fraction by flow cytometry. A titration assay was performed to determine the PK parameters, and the obtained parameter was comparable to that determined by the fitting of the in vivo PK. This approach was also extended to NPC from monkeys. The concentration-dependent binding and uptake was measured to determine the PK parameters using monkey NPC, the FcγRIIB-expressing fraction of which was identified by CD31 and CD45. The findings presented herein demonstrate that the in vitro liver NPC assay using flow cytometry is a useful tool to determine the binding and uptake of biologics and to predict the PK.

scholarly journals Fractionation of Hepatic Nonparenchymal Cells

2002 ◽  
Vol 2 ◽  
pp. 1347-1350 ◽  
Author(s):  
John Graham
Keyword(s):  
Endothelial Cells ◽  
Stellate Cells ◽  
Cell Types ◽  
Low Density ◽  
Nonparenchymal Cells ◽  
Mammalian Liver ◽  
Hepatic Nonparenchymal Cells ◽  
Density Barrier ◽  
Parenchymal Cells ◽  
Different Cell Types

The majority of parenchymal cells from mammalian liver cells can be removed by very low speed centrifugation (50 g) but a simple low-density barrier (1.096 g/ml) is required to remove the remaining parenchymal cells from the 50-g supernatant which contains all of the lower density nonparenchymal cells. Continuous gradients of Nycodenz®can provide satisfactory resolution of Kupffer, stellate, and endothelial cells on an analytical basis but the separation of different cell types is not sufficient preparatively. Flotation through a low-density iodixanol barrier can, however, provide a satisfactory enrichment of the least dense nonparenchymal cell – the stellate cells.

Erythrophagocytosis by Entamoeba histolytica.- Ultrastructural Study

1972 ◽  
Vol 30 ◽  
pp. 156-157 ◽  
Author(s):  
Norberto Treviño ◽  
Alfredo Feria-Velasco ◽  
I. Ruiz de Chávez
Keyword(s):  
Electron Microscopy ◽  
Light Microscopy ◽  
Entamoeba Histolytica ◽  
Ultrastructural Study ◽  
Saline Solution ◽  
Physiological Saline ◽  
Ultrastructural Level ◽  
Hot Plate ◽  
Physiological Saline Solution ◽  
Axenic Conditions

Although erythrophagocytosis by various species of Entamoeba is a well known phenomenon this has not yet been studied in detail at the ultrastructural level. The present work deals with the description of the incorporation process of erythrocytes by trophozoites of E. histolytica. For this study, trophozoites of E. histolytica, HK-9:NIH strain cultured in axenic conditions and washed human erythrocytes were placed on a hot plate at 37°C in physiological saline solution. After 5 minutes, 2.5% glutarldehyde was added and the samples were processed according to conventional techniques for electron microscopy.Based upon light microscopy studies on living trophozoites in contact with erythrocytes, it seems that erythrophagocytosis only takes place in one pole of the parasite.

scholarly journals Delivery of Therapeutic Agents to the Central Nervous System and the Promise of Extracellular Vesicles

Pharmaceutics ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 492
Author(s):  
Charlotte A. René ◽  
Robin J. Parks
Keyword(s):  
Central Nervous System ◽  
Endothelial Cells ◽  
Nervous System ◽  
Blood Brain Barrier ◽  
Extracellular Vesicles ◽  
Therapeutic Agents ◽  
Target Cells ◽  
Significant Barrier ◽  
The Central Nervous System ◽  
Delivery Vehicles

The central nervous system (CNS) is surrounded by the blood–brain barrier (BBB), a semipermeable border of endothelial cells that prevents pathogens, solutes and most molecules from non-selectively crossing into the CNS. Thus, the BBB acts to protect the CNS from potentially deleterious insults. Unfortunately, the BBB also frequently presents a significant barrier to therapies, impeding passage of drugs and biologicals to target cells within the CNS. This review provides an overview of different approaches to deliver therapeutics across the BBB, with an emphasis in extracellular vesicles as delivery vehicles to the CNS.

scholarly journals The distribution, induction and isoenzyme profile of glutathione S-transferase and glutathione peroxidase in isolated rat liver parenchymal, Kupffer and endothelial cells

1989 ◽  
Vol 264 (3) ◽  
pp. 737-744 ◽  
Author(s):  
P Steinberg ◽  
H Schramm ◽  
L Schladt ◽  
L W Robertson ◽  
H Thomas ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Glutathione Peroxidase ◽  
Rat Liver ◽  
Peroxidase Activity ◽  
Cell Types ◽  
Transferase Activity ◽  
Glutathione Peroxidase Activity ◽  
Glutathione S Transferase ◽  
Liver Parenchymal ◽  
Parenchymal Cells

The distribution and inducibility of cytosolic glutathione S-transferase (EC 2.5.1.18) and glutathione peroxidase (EC 1.11.1.19) activities in rat liver parenchymal, Kupffer and endothelial cells were studied. In untreated rats glutathione S-transferase activity with 1-chloro-2,4-dinitrobenzene and 4-hydroxynon-2-trans-enal as substrates was 1.7-2.2-fold higher in parenchymal cells than in Kupffer and endothelial cells, whereas total, selenium-dependent and non-selenium-dependent glutathione peroxidase activities were similar in all three cell types. Glutathione S-transferase isoenzymes in parenchymal and non-parenchymal cells isolated from untreated rats were separated by chromatofocusing in an f.p.l.c. system: all glutathione S-transferase isoenzymes observed in the sinusoidal lining cells were also detected in the parenchymal cells, whereas Kupffer and endothelial cells lacked several glutathione S-transferase isoenzymes present in parenchymal cells. At 5 days after administration of Arocolor 1254 glutathione S-transferase activity was only enhanced in parenchymal cells; furthermore, selenium-dependent glutathione peroxidase activity decreased in parenchymal and non-parenchymal cells. At 13 days after a single injection of Aroclor 1254 a strong induction of glutathione S-transferase had taken place in all three cell types, whereas selenium-dependent glutathione peroxidase activity remained unchanged (endothelial cells) or was depressed (parenchymal and Kupffer cells). Hence these results clearly establish that glutathione S-transferase and glutathione peroxidase are differentially regulated in rat liver parenchymal as well as non-parenchymal cells. The presence of glutathione peroxidase and several glutathione S-transferase isoenzymes capable of detoxifying a variety of compounds in Kupffer and endothelial cells might be crucial to protect the liver from damage by potentially hepatotoxic substances.

scholarly journals Chimeric Maternal Cells with Tissue-Specific Antigen Expression and Morphology Are Common in Infant Tissues

2009 ◽  
Vol 12 (5) ◽  
pp. 337-346 ◽  
Author(s):  
Anne M. Stevens ◽  
Heidi M. Hermes ◽  
Meghan M. Kiefer ◽  
Joe C. Rutledge ◽  
J. Lee Nelson
Keyword(s):  
Islet Cells ◽  
Tissue Injury ◽  
Specific Antigen ◽  
Antigen Expression ◽  
Cell Types ◽  
Target Cells ◽  
Specific Cell ◽  
Tissue Specific ◽  
Renal Tubular Cells ◽  
Parenchymal Cells

Maternal microchimerism (MMc) has been purported to play a role in the pathogenesis of autoimmunity, but how a small number of foreign cells could contribute to chronic, systemic inflammation has not been explained. Reports of peripheral blood cells differentiating into tissue-specific cell types may shed light on the problem in that chimeric maternal cells could act as target cells within tissues. We investigated MMc in tissues from 7 male infants. Female cells, presumed maternal, were characterized by simultaneous immunohistochemistry and fluorescence in situ hybridization for X- and Y-chromosomes. Maternal cells constituted 0.017% to 1.9% of parenchymal cells and were found in all infants in liver, pancreas, lung, kidney, bladder, skin, and spleen. Maternal cells were differentiated: maternal hepatocytes in liver, renal tubular cells in kidney, and β-islet cells in pancreas. Maternal cells were not found in areas of tissue injury or inflammatory infiltrate. Maternal hematopoietic cells were found only in hearts from patients with neonatal lupus. Thus, differentiated maternal cells are present in multiple tissue types and occur independently of inflammation or tissue injury. Loss of tolerance to maternal parenchymal cells could lead to organ-specific “auto” inflammatory disease and elimination of maternal cells in areas of inflammation.

scholarly journals Molecular mechanisms of microvascular failure in central nervous system injury—synergistic roles of NKCC1 and SUR1/TRPM4

2010 ◽  
Vol 113 (3) ◽  
pp. 622-629 ◽  
Author(s):  
J. Marc Simard ◽  
Kristopher T. Kahle ◽  
Volodymyr Gerzanich
Keyword(s):  
Endothelial Cells ◽  
Cerebral Edema ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion ◽  
Extracellular Fluid ◽  
Inflammatory Cells ◽  
Atp Depletion ◽  
Energy Status ◽  
Edema Formation ◽  
Trpm4 Channel

Microvascular failure largely underlies the damaging secondary events that accompany traumatic brain injury (TBI). Changes in capillary permeability result in the extravasation of extracellular fluid, inflammatory cells, and blood, thereby producing cerebral edema, inflammation, and progressive secondary hemorrhage (PSH). Recent work in rat models of TBI and stroke have implicated 2 ion transport proteins expressed in brain endothelial cells as critical mediators of edema formation: the constitutively expressed Na+-K+-2Cl– cotransporter, NKCC1, and the trauma/ischemia-induced SUR1-regulated NCCa-ATP (SUR1/TRPM4) channel. Whereas NKCC1 function requires adenosine 5′-triphosphate (ATP), activation of SUR1/TRPM4 occurs only after ATP depletion. This opposite dependence on intracellular ATP levels implies that one or the other mechanism will activate/deactivate as ATP concentrations rise and fall during periods of ischemia/reperfusion, resulting in continuous edema formation regardless of cellular energy status. Moreover, with critical ATP depletion, sustained opening of SUR1/TRPM4 channels results in the oncotic death of endothelial cells, leading to capillary fragmentation and PSH. Bumetanide and glibenclamide are 2 well-characterized, safe, FDA-approved drugs that inhibit NKCC1 and the SUR1/TRPM4 channel, respectively. When used alone, these drugs have provided documented beneficial effects in animal models of TBI- and ischemiaassociated cerebral edema and PSH. Given the mechanistic and temporal differences by which NKCC1 and the SUR1/TRPM4 channel contribute to the pathophysiological mechanisms of these events, combination therapy with bumetanide and glibenclamide may yield critical synergy in preventing injury-associated capillary failure.

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