An ultrastructural study on the role of Kupffer cells in the process of infection by Plasmodium berghei sporozoites in rats

SUMMARYThe interactions in vivo between Plasmodium berghei sporozoites and Kupffer cells in rat livers were studied by transmission electron microscopy. By 10 and 15 min after inoculation, sporozoites were both free in the liver sinusoids and inside endocytotic vacuoles of the Kupffer cells. The latter cells were very active in phagocytosing sporozoites, bacteria and red blood cells. The sporozoites retained their integrity inside the endocytotic vacuoles and no signs of lysosomal digestion were observed. Sporozoites seen within endocytotic vacuoles 1 h after inoculation were still morphologically intact, although bristle-coated vesicles fused with the vacuole membrane. Evidence is presented which suggests that Kupffer cells transport sporozoites towards the space of Disse and adjacent hepatocytes. No sporozoites were seen to penetrate an endothelial cell or its narrow fenestrae. It is proposed that Kupffer cell passage, rather than gaps in the sinusoidal lining, represents the normal route that sporozoites take to circumvent the endothelial barrier. The localization of exo-erythrocytic forms was made easier by the use of Brown Norway rats in which many more parasites develop than in the Wistar rats. The distribution pattern of the parasites was found to be mainly around the ‘periportal’ zones of the acini of liver tissue.

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Inhibitory action of Wnt target gene osteopontin on mitochondrial cytochrome c release determines renal ischemic resistance

AJP Renal Physiology ◽

10.1152/ajprenal.00687.2009 ◽

2010 ◽

Vol 299 (1) ◽

pp. F234-F242 ◽

Cited By ~ 10

Author(s):

Jose Luis Viñas ◽

Anna Sola ◽

Michaela Jung ◽

Chrysoula Mastora ◽

Eugenia Vinuesa ◽

...

Keyword(s):

Cytochrome C ◽

Wnt Pathway ◽

Brown Norway ◽

Mitochondrial Cytochrome ◽

Cytochrome C Release ◽

Norway Rats ◽

Mitochondrial Cytochrome C

Certain determinants of ischemic resistance in the Brown Norway rat strain have been proposed, but no studies to date have focused on the role of the Wnt pathway in the ischemic resistance mechanism. We performed a comparative genomic study in Brown Norway vs. Sprague-Dawley rats. Selective manipulations of the Wnt pathway in vivo and in vitro allowed us to study whether the action of the Wnt pathway on apoptosis through the regulation of osteopontin was critical to the maintenance of inherent ischemic resistance mechanisms. The results revealed a major gene upregulation of the Wnt family in Brown Norway rats after renal ischemia-reperfusion. Manipulation of the Wnt signaling cascade by selective antibodies increased mitochondrial cytochrome c release and caspase 3 activity. The antiapoptotic role of Wnt was mediated by osteopontin, a direct Wnt target gene. Osteopontin was reduced by Wnt antibody administration in vivo, and osteopontin gene silencing in vitro significantly increased mitochondrial cytochrome c release. The overexpression of Wnt pathway genes detected in Brown Norway rats is critical in the maintenance of their inherent ischemic resistance. Activation of the Wnt signaling cascade reduces mitochondrial cytochrome c release and caspase 3 activity through the action of osteopontin.

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Evidence for Kupffer cell migration along liver sinusoids, from high-resolution in vivo microscopy

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1992.263.1.g17 ◽

1992 ◽

Vol 263 (1) ◽

pp. G17-G23 ◽

Cited By ~ 8

Author(s):

P. J. MacPhee ◽

E. E. Schmidt ◽

A. C. Groom

Keyword(s):

High Resolution ◽

Kupffer Cells ◽

Fluorescent Microspheres ◽

Fixed Tissue ◽

Liver Sinusoids ◽

Quantitative Measurements ◽

The Mean ◽

Antigen Presenting

Kupffer cells are generally considered fixed tissue macrophages of the liver. However, we have evidence that this opinion is incorrect. High-resolution in vivo video microscopy shows that Kupffer cells have the ability to migrate along sinusoidal walls. Images recorded from anesthetized mice show active locomotion of cells with or against the direction of blood flow or in the absence of flow. The size, changing morphology, and uptake of carbon or microspheres strongly suggest that these are Kupffer cells. Quantitative measurements were made on 29 migrating Kupffer cells. The mean speed of migration was 4.6 +/- 2.6 (SD) microns/min and was not significantly different whether migration occurred with or against the flow. When fluorescent microspheres were given in vivo as a phagocytic challenge, Kupffer cells containing few microspheres migrated more slowly (0.9 +/- 0.9 microns/min, n = 10), whereas those containing many microspheres were never seen to migrate. Individual Kupffer cells were able to move independently, i.e., in directions different from those of neighboring Kupffer cells. These findings may have major implications for the role of Kupffer cells in scavenging foreign particles and as antigen-presenting cells.

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THE INTERACTION OF BLOOD ELEMENTS WITH ENDOCARDIAL ENDOTHELIUM DAMAGED BY LACTIC ACID

10.1055/s-0038-1643548 ◽

1987 ◽

Author(s):

G Carter ◽

B J Gavin

Keyword(s):

Lactic Acid ◽

Basal Lamina ◽

Myocardial Infarct ◽

Transmission Electron ◽

Rat Hearts ◽

Cacodylate Buffer ◽

Aortic Cannula ◽

Endocardial Endothelium

It has already been demonstrated that ischaemic metabolites, which could diffuse frcm a myocardial infarct in vivo, can cause substantial damage to the endocardial endotheliun and this could predispose to mural thrombosis.To investigate the role of ischaemic metabolites in the pathogenesis of mural thrombosis, lactic acid (pH6.4) was passed through a two-way concentric catheter ligated into the left ventricle of isolated beating rat hearts that were perfused with oxygenated Krebs-Henseleit buffer (KHB) through an aortic cannula. After periods of 1, 2, and 4 hours, the lactic acid was followed for 10 minutes by 10 mis of whole blood from hepa-rinized donor rats. Ventricles were then flushed with KHB, fixed in 2.5% glutaraldehyde and post-fixed in 1% osmium tetrox-ide in cacodylate buffer.Scanning and transmission electron microscopy showed that platelets adhered to exposed basal lamina, microfibrils and collagen but not to intact or damaged endothelial cells. However densely aggregated thrombi only farmed on regions of exposed connective tissue and never on basal lamina. Fibrin, leukocytes and red blood cells were associated with these platelet thrombi. Thus lactic acid and other ischaemic metabolites which could possibly diffuse in vivo from an infarct can contribute to endocardial damage which predisposes to mural thrombosis.

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Role of ICAM-1 in chronic hepatic allograft rejection in the rat

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00222.2001 ◽

2002 ◽

Vol 283 (1) ◽

pp. G196-G203 ◽

Cited By ~ 7

Author(s):

John Wong ◽

Paul Kubes ◽

Yikun Zhang ◽

Yang Li ◽

Stefan J. Urbanski ◽

...

Keyword(s):

Allograft Rejection ◽

Leukocyte Adhesion ◽

Leukocyte Recruitment ◽

Intercellular Adhesion Molecule ◽

Brown Norway ◽

Intercellular Adhesion Molecule 1 ◽

Cell Recruitment ◽

Hepatic Allograft

The pathogenesis of hepatic allograft rejection remains unclear. We aimed to clarify the early role of intercellular adhesion molecule-1 (ICAM-1)-mediated cell recruitment in chronic hepatic rejection. Liver transplantation was performed from Lewis to Lewis rats (isograft controls) and from Lewis to Brown Norway rats (allograft rejection group). The allografted rats were treated with either ICAM-1 antisense oligonucleotides (10 mg · kg−1· day−1× 6 days ip) or a control preparation (either ICAM-1 missense oligonucleotide or normal saline). Hepatic leukocyte recruitment in vivo was studied on day 6 by using intravital microscopy. Liver histology, biochemistry, and survival rates were also examined. Leukocyte adhesion in terminal hepatic venules was significantly increased in the rejection group compared with isograft controls. Antisense ICAM-1 in the allografted group effectively reduced leukocyte adhesion. Histology and liver chemistry were less deranged in the antisense-treated groups compared with control-treated allografted rats. In the allograft groups, survival was significantly prolonged in the antisense-treated rats (42.3 ± 1.2 days) compared with the controls (25.2 ± 2.7 days). These results showed that early leukocyte recruitment in the hepatic microvasculature of rejecting allografts is ICAM-1 dependent and suggest that impacting on early cell recruitment can significantly ameliorate chronic rejection.

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Sustained scleral stiffening in rats after a single genipin treatment

Journal of The Royal Society Interface ◽

10.1098/rsif.2019.0427 ◽

2019 ◽

Vol 16 (159) ◽

pp. 20190427 ◽

Cited By ~ 2

Author(s):

Bailey G. Hannon ◽

Stephen A. Schwaner ◽

Elizabeth M. Boazak ◽

Brandon G. Gerberich ◽

Erin J. Winger ◽

...

Keyword(s):

Digital Image Correlation ◽

Digital Image ◽

Image Correlation ◽

Brown Norway ◽

Post Injection ◽

Functional Studies ◽

Multiple Treatments ◽

Lagrange Strain ◽

Norway Rats

Scleral stiffening has been proposed as a therapy for glaucoma and myopia. Previous in vivo studies have evaluated the efficacy of scleral stiffening after multiple treatments with a natural collagen crosslinker, genipin. However, multiple injections limit clinical translatability. Here, we examined whether scleral stiffening was maintained after four weeks following a single genipin treatment. Eyes from brown Norway rats were treated in vivo with a single 15 mM genipin retrobulbar injection, sham retrobulbar injection, or were left naive. Eyes were enucleated either 1 day or four weeks post-injection and underwent whole globe inflation testing. We assessed first principal Lagrange strain of the posterior sclera using digital image correlation as a proxy for scleral stiffness. Four weeks post-injection, genipin treatment resulted in a 58% reduction in scleral strain as compared to controls ( p = 0.005). We conclude that a single in vivo injection of genipin effectively stiffened rat sclera for at least four weeks which motivates further functional studies and possible clinical translation of genipin-induced scleral stiffening.

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Kupffer cells from carbon tetrachloride–injured rat livers produce chemotactic factors for fibroblasts and monocytes: The role of tumor necrosis factor-α

Hepatology ◽

10.1002/hep.1840140523 ◽

1991 ◽

Vol 14 (5) ◽

pp. 895-900 ◽

Cited By ~ 22

Author(s):

Juan Armendariz-Borunda ◽

Jerome M. Seyer ◽

Arnold E. Postlethwaite ◽

Andrew H. Kang

Keyword(s):

Carbon Tetrachloride ◽

Tumor Necrosis Factor ◽

Kupffer Cells ◽

Tumor Necrosis ◽

Tumor Necrosis Factor Α ◽

Chemotactic Factors ◽

Factor Α ◽

Rat Livers ◽

Necrosis Factor

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Role of sodium silicate in induction of scleroderma-related autoantibodies in brown Norway rats through oral and subcutaneous administration

Rheumatology International ◽

10.1007/s00296-009-1327-3 ◽

2010 ◽

Vol 31 (5) ◽

pp. 611-615 ◽

Cited By ~ 7

Author(s):

Sultan M. Al-Mogairen

Keyword(s):

Sodium Silicate ◽

Subcutaneous Administration ◽

Brown Norway ◽

Norway Rats

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Surface-induced formation and redox-dependent staining of outer membrane extensions inShewanella oneidensisMR-1

10.1101/689703 ◽

2019 ◽

Author(s):

Grace W. Chong ◽

Sahand Pirbadian ◽

Mohamed Y. El-Naggar

Keyword(s):

Outer Membrane ◽

Shewanella Oneidensis ◽

Medium Composition ◽

Extracellular Electron Transfer ◽

Active Components ◽

Transmission Electron ◽

Redox Active ◽

Redox Centers

AbstractThe metal-reducing bacteriumShewanella oneidensisMR-1 produces extensions of its outer membrane (OM) and periplasm that contain cytochromes responsible for extracellular electron transfer (EET) to external redox-active surfaces, including minerals and electrodes. While the role of multi-heme cytochromes in transporting electrons across the cell wall is well established, their distribution alongS. oneidensisOM extensions is also thought to allow lateral electron transport along these filaments. These proposed bacterial nanowires, which can be several times the cell length, would thereby extend EET to more distant electron acceptors. However, it is still unclear why these extensions form, and to what extent they contribute to respiration in living cells. Here, we investigate physical contributors to their formation usingin vivofluorescence microscopy. While previous studies focused on the display ofS. oneidensisouter membrane extensions (OMEs) as a response to oxygen limitation, we find that cell-to-surface contact is sufficient to trigger the production of OMEs, including some that reach >100 µm in length, irrespective of medium composition, agitation, or aeration. To visualize the extent of heme redox centers along OMEs, and help distinguish these structures from other extracellular filaments, we also performed histochemical redox-dependent staining with transmission electron microscopy on wild type and cytochrome-deficient strains. We demonstrate that redox-active components are limited to OMEs and not present on other extracellular appendages, such as pili and flagella. We also observed that the loss of 8 functional periplasmic and outer membrane cytochromes significantly decreased both the frequency and intensity of redox-dependent staining found widespread on OMEs. These results will improve our understanding of the environmental conditions that influence the formation ofS. oneidensisOMEs, as well as the distribution and functionality of EET components along extracellular appendages.

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The surface (S-) layer is a virulence factor of Bacteroides forsythus

Microbiology ◽

10.1099/mic.0.26535-0 ◽

2003 ◽

Vol 149 (12) ◽

pp. 3617-3627 ◽

Cited By ~ 74

Author(s):

M. Sabet ◽

S.-W. Lee ◽

R. K. Nauman ◽

T. Sims ◽

H.-S. Um

Keyword(s):

Virulence Factor ◽

Systemic Disease ◽

Periodontal Pathogen ◽

Whole Cells ◽

Virulence Potential ◽

Transmission Electron ◽

Immunization Study ◽

Antibody Inhibition

Bacteroides forsythus has emerged as a crucial periodontal pathogen with possible implications for systemic disease. The aim of this study was to isolate the S-layer from B. forsythus and examine its virulence potential as a part of efforts to characterize virulence factors of B. forsythus. The role of the S-layer in the haemagglutinating and adherent/invasive activities was evaluated. It was observed that the S-layer alone was able to mediate haemagglutination. In adherent and invasive studies, transmission electron microscopy clearly revealed that B. forsythus cells were able to attach to and invade KB cells, showing the formation of a microvillus-like extension around adherent and intracellular bacteria. The quantitative analysis showed that five different B. forsythus strains exhibited attachment (1·9–2·3 %) and invasion (0·4–0·7 %) capabilities. It was also observed through antibody inhibition assays that adherent/invasive activities of B. forsythus are mediated by the S-layer. Furthermore, an in vivo immunization study adopting a murine abscess model was used to prove that the S-layer is involved in the infectious process of abscess formation. While mice immunized with purified S-layer and B. forsythus whole cells did not develop any abscesses when challenged with viable B. forsythus cells, unimmunized mice developed abscesses. Collectively, the data obtained from these studies indicate that the S-layer of B. forsythus is a virulence factor.

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