scholarly journals Incidence of Apoptosis in the Lymphoid Organs of Normal or Malaria Infected Mice is Decreased in CD18 and Urokinase - Receptor (UPAR, CD87) Deficient Mice

2001 ◽  
Vol 8 (3-4) ◽  
pp. 183-191 ◽  
Author(s):  
Pierre Francois Piguet ◽  
Chen da Laperrousaz ◽  
Christian Vesin ◽  
Yves Donati
Keyword(s):  
Lymph Nodes ◽  
Annexin V ◽  
Urokinase Receptor ◽  
Lymphoid Organs ◽  
White Pulp ◽  
Facs Analysis ◽  
Surface Molecules ◽  
Spleen And Lymph Nodes ◽  
Serum Igg Levels ◽  
Deficient Mice

Incidence of apoptosis was investigated in the spleen and lymph nodes of +/+, CD18 -/- and urokinase receptor (uPAR, CD87) -/- mice, untreated orPlasmodium Berghei Anka(PbA) infected. In non infected mice, incidence of apoptosis was lower in the lymph nodes of CD18 -/- and uPAR -/- than in +/+ mice, as seen by FACS analysis to count the number of hypodiploid and Annexin-V binding cells. Infection of mice with PbA resulted in a marked increase in the size of spleen and lymph nodes 7–8 days after infection, which was slightly higher in uPAR -/- and CD18 -/- than in +/+ mice. PbA infection increased about 7 fold the incidence of apoptosis in the lymphoid organs of +/+, especially in the white pulp and germinal centers of the spleen and lymph nodes, while in contrast it was unchanged in PbA infected CD18 -/- or uPAR -/- mice. Serum IgG levels, and number of circulating leukocytes were significantly higher in both uPAR and CD18 -/- than in +/+ mice. These results indicate that the CD18 and uPAR surface molecules, which are known to be associated in the cell membrane, have an important influence upon the incidence of cell survival in both normal or stimulated lymphoid organs.

scholarly journals Cyclical modulation of sphingosine-1-phosphate receptor 1 surface expression during lymphocyte recirculation and relationship to lymphoid organ transit

2005 ◽  
Vol 201 (2) ◽  
pp. 291-301 ◽  
Author(s):  
Charles G. Lo ◽  
Ying Xu ◽  
Richard L. Proia ◽  
Jason G. Cyster
Keyword(s):  
Lymph Nodes ◽  
Surface Expression ◽  
Lymphoid Organ ◽  
Lymphoid Organs ◽  
White Pulp ◽  
Activated T Cells ◽  
Circulating Lymphocytes ◽  
Sphingosine 1 Phosphate ◽  
Splenic White Pulp ◽  
Lymphocyte Egress

Sphingosine-1-phosphate receptor 1 (S1P1) was recently shown to be required for lymphocyte egress from lymphoid organs. Here we have examined the relationship between S1P1 abundance on the cell and egress efficiency. Using an integrin neutralization approach to separate the processes of entry and exit, we show that pertussis toxin treatment reduces lymphocyte egress from lymph nodes. Retrovirally mediated S1P1 overexpression is sufficient to reduce B cell accumulation in the splenic white pulp and to promote egress of activated T cells from lymph nodes, whereas S1P1+/−cells have reduced lymph node exit efficiency. Furthermore, lymphocyte S1P1 is down-regulated in the blood, up-regulated in lymphoid organs, and down-regulated again in the lymph. We propose that cyclical ligand-induced modulation of S1P1 on circulating lymphocytes contributes to establishing their lymphoid organ transit time.

scholarly journals Histological and histochemical changes in the peripheral organs of the immune system of dogs in cases of isoniazid poisoning

2021 ◽  
Vol 12 (3) ◽  
pp. 537-544
Author(s):  
G. I. Kotsyumbas ◽  
N. P. Vretsona
Keyword(s):  
Immune System ◽  
Lymph Nodes ◽  
Clinical Course ◽  
Clinical Diagnostics ◽  
Pathological Examination ◽  
White Pulp ◽  
Peripheral Organs ◽  
Vascular Walls ◽  
Spleen And Lymph Nodes ◽  
Histochemical Changes

Most publications on isoniazid poisoning in dogs are devoted to clinical diagnostics, treatment, and prevention of the disease. Histological and histochemical changes are not fully described, though they are important in assessing the toxic effects of isoniazid. Isoniazid is used to treat tuberculosis in humans. Dogs are hypersensitive to this drug. The article highlights the results of macroscopic, histological, and histochemical studies of the dogs’ lymph nodes and spleen in cases of isoniazid poisoning. A pathological examination of 19 corpses of dogs of different ages was performed, during which isoniazid poisoning was posthumously diagnosed, based on anamnesis, clinical signs, pathological autopsy, histological, and histochemical examination. Samples of lymph nodes and spleen were fixed in a 10% aqueous neutral formalin solution, Carnoy’s solution, and Bouin’s fixative. Histoсuts were prepared using a sled microtome and stained with hematoxylin and eosin. Staining was also performed according to the techniques suggested by McManus, Brachet, and Perls. The pathomorphological changes in lymph nodes and spleen were characterized by disorganization of vascular walls and connective tissue fibers of the stroma, dilatation of veins, their overflow with hemolyzed blood, and, in cases of the long clinical course, thrombosis of small vessels. Intravascular hemolysis of erythrocytes resulted in an excessive formation of hemosiderin. Histochemically, the spleen and lymph nodes showed a significant increase in the number of hemosiderophages in the spleen’s red and white pulp and the lymph nodes’ central sinuses and pulp cords. In the spleen, mucoid swelling and necrobiotic changes in the wall structures of the arterioles and arteries progressed with a narrowing of their lumen in dogs suffering from the long clinical course. Increased permeability of the microcirculatory tract vessels of the spleen and lymph nodes, transudate formation, and the destructive changes in the reticular skeleton accompanied hemodynamic violations. A sharp change in blood rheology caused the violation of trophism and metabolism in the immune system. Lymphoid elements of the lymph nodes and white pulp of the spleen were in a state of karyorrhexis and karyolysis. The morphological study of the immune system’s peripheral organs suggests that dogs poisoned by isoniazid demonstrate hemodynamic disorders, changes in the physicochemical properties of blood (hemolysis of erythrocytes and thrombosis). This is the basis of trophic disorders, metabolic malfunctions, and the development of dystrophic processes in all structural elements of the spleen and lymph nodes.

scholarly journals Deoxynivalenol in the liver and lymphoid organs of rats: effects of dose and duration on immunohistological changes

2017 ◽  
Vol 10 (1) ◽  
pp. 89-96 ◽  
Author(s):  
A.P.F.L. Bracarense ◽  
K.M. Basso ◽  
E.O. Da Silva ◽  
D. Payros ◽  
I.P. Oswald
Keyword(s):  
Lymph Nodes ◽  
Control Diet ◽  
Lymphoid Organs ◽  
Hepatocyte Proliferation ◽  
Dependent Manner ◽  
Histological Changes ◽  
Lymphoid Depletion ◽  
Spleen And Lymph Nodes ◽  
Cytoplasmic Vacuolisation ◽  
Immunohistochemical Analyses

Deoxynivalenol (DON) is one of the most prevalent type B trichothecenes present in food inducing adverse effects, including intestinal changes and immunosuppression. The aim of the present study was to investigate the effects of DON on rats exposed for 7, 14 and 28 days to mycotoxin-contaminated diets, using histological and immunohistochemical analyses on liver and lymphoid organs. Fifty rats received a control diet, or a diet contaminated with 1.75 mg/kg of DON for 30 days, or a diet contaminated with 11.4 mg/kg of DON for 7, 14 or 30 days. Ingestion of contaminated feed induced a significant increase in the lesional score in the liver, spleen, and lymph nodes. The main histological findings observed in the liver were cytoplasmic vacuolisation and hepatocelular megalocytosis. A significant increase in hepatocyte proliferation was observed in rats that received 1.75 mg/kg of DON. Lymphoid depletion was the main histological alteration observed in lymphoid organs, resulting in a significant increase in the lesional score in all groups that received the contaminated diets. The histological changes and lymphocyte apoptosis were more severe in lymph nodes of rats fed 11.4 mg/kg of DON during 30 days. The results of the morphological and immunohistochemical analyses suggest that the ingestion of DON can induce functional hepatic impairment and immunosuppression in a dose- and time-dependent manner.

THE EFFECT OF HYPOPHYSECTOMY, ADRENALECTOMY AND CORTISONE ON THE INCORPORATION OF TRITIATED THYMIDINE IN RAT ORGANS, WITH SPECIAL REFERENCES TO THE LYMPHOID TISSUES

1966 ◽  
Vol 53 (3) ◽  
pp. 519-528 ◽  
Author(s):  
F. Knutson ◽  
P. M. Lundin
Keyword(s):  
Lymph Nodes ◽  
Tritiated Thymidine ◽  
Lymphoid Organs ◽  
Prolonged Treatment ◽  
Lymphoid Tissues ◽  
Rat Organs ◽  
Spleen And Lymph Nodes ◽  
Apparent Influence

ABSTRACT After hypophysectomy, the incorporation of tritiated thymidine decreases in the thymus and spleen, but not in the lymph nodes. Adrenalectomy has no apparent influence on this incorporation. After prolonged treatment with moderate amounts of cortisone, the incorporation is significantly decreased in the thymus and spleen, but the slight decrease in the lymph nodes is not significant. In untreated animals the incorporation is of the same magnitude in all three lymphoid tissues. These results are compared with those obtained with 32P O4 – a method that gives a relatively higher incorporation in the thymus than in the spleen and lymph nodes. These values are more consistent with the mitotic indices of these organs. The reutilization of thymidine in the lymphoid organs is discussed. It is concluded that such a reutilization is a normal mechanism in the lymphoid tissues, and that it is markedly increased while under the influence of corticosteroids, particularly in the thymus.

scholarly journals The Reduced Expression of 6ckine in the plt Mouse Results from the Deletion of One of Two 6ckine Genes

1999 ◽  
Vol 190 (8) ◽  
pp. 1183-1188 ◽  
Author(s):  
Galya Vassileva ◽  
Hortensia Soto ◽  
Albert Zlotnik ◽  
Hideki Nakano ◽  
Terutaka Kakiuchi ◽  
...  
Keyword(s):  
T Cells ◽  
Lymph Node ◽  
T Cell ◽  
T Lymphocytes ◽  
Lymph Nodes ◽  
Lymphoid Organs ◽  
Peyer's Patches ◽  
White Pulp ◽  
Naive T Lymphocytes

6Ckine is an unusual chemokine capable of attracting naive T lymphocytes in vitro. It has been recently reported that lack of 6Ckine expression in lymphoid organs is a prominent characteristic of mice homozygous for the paucity of lymph node T cell (plt) mutation. These mice show reduced numbers of T cells in lymph nodes, Peyer's patches, and the white pulp of the spleen. The genetic reason for the lack of 6Ckine expression in the plt mouse, however, has remained unknown. Here we demonstrate that mouse 6Ckine is encoded by two genes, one of which is expressed in lymphoid organs and is deleted in plt mice. A second 6Ckine gene is intact and expressed in the plt mouse.

scholarly journals Cooperating Mechanisms of CXCR5 and CCR7 in Development and Organization of Secondary Lymphoid Organs

2003 ◽  
Vol 197 (9) ◽  
pp. 1199-1204 ◽  
Author(s):  
Lars Ohl ◽  
Golo Henning ◽  
Stefan Krautwald ◽  
Martin Lipp ◽  
Svenja Hardtke ◽  
...  
Keyword(s):  
Functional Organization ◽  
Mesenchymal Cells ◽  
Lymphoid Organ ◽  
Lymphoid Organs ◽  
White Pulp ◽  
Organ Development ◽  
Secondary Lymphoid Organ ◽  
Small Clusters ◽  
Secondary Lymphoid Organs ◽  
Deficient Mice

Homeostatic chemokines participate in the development of secondary lymphoid organs and later on in the functional organization of these tissues. The development of lymph nodes (LNs) and Peyer's patches depends on the recruitment of CD3− CD4+ interleukin (IL)-7Rαhi cells to sites of future organ development. CD3− CD4+ IL-7Rαhi cells express the chemokine receptor CXCR5 and might be attracted by its ligand CXCL13, which is secreted by mesenchymal cells. Mesenchymal cells also secrete CCL19, a ligand for CCR7, yet it is not clear whether CCR7 and CCL19 are important for secondary lymphoid organ development. Analyzing CXCR5−/− CCR7−/− double deficient mice we now show that these mice lack all examined peripheral LNs suggesting a profound role for both receptors in secondary lymphoid organ development. We demonstrate that CD3− CD4+ IL-7Rαhi cells express CXCR5 as well as CCR7 indicating that both receptors cooperate during an early step of secondary lymphoid organ development. Furthermore, CXCR5−/− CCR7−/− mice display a severely disturbed architecture of mesenteric LN and spleen. Due to an impaired migration of B cells into the white pulp, CXCR5−/− CCR7−/− mice fail to develop B cell follicles but show small clusters of unorganized lymphocytes in the spleen. These data demonstrate a cooperative function of CXCR5 and CCR7 in lymphoid organ organogenesis and organization.

scholarly journals Defective Peyer's patch organogenesis in mice lacking the 55-kD receptor for tumor necrosis factor.

1996 ◽  
Vol 184 (1) ◽  
pp. 259-264 ◽  
Author(s):  
B Neumann ◽  
A Luz ◽  
K Pfeffer ◽  
B Holzmann
Keyword(s):  
Tumor Necrosis Factor ◽  
Lymph Nodes ◽  
Tumor Necrosis ◽  
Peyer's Patches ◽  
Mutant Mice ◽  
Peyer’S Patches ◽  
White Pulp ◽  
Genetic Ablation ◽  
Deficient Mice ◽  
Necrosis Factor

Lymphotoxin alpha (LT-alpha) may form secreted homotrimers binding to p55 and p75 tumor necrosis factor (TNF) receptors or cell surface-bound heterotrimers with LT-beta that interact with the LT-beta receptor. Genetic ablation of LT-alpha revealed that mutant mice have no detectable lymph nodes or Peyer's patches and that the organization of the splenic white pulp in T and B cell areas is disturbed. In this report we describe a novel function for the p55 TNF receptor during ontogeny and demonstrate that mice deficient for p55 completely lack organized Peyer's patches. In contrast, lymph nodes and spleen are present in p55-deficient mice and lymphocytes segregate normally into B and T cell areas in these organs. Lamina propria and intraepithelial lymphocytes of the small intestine were detected in normal number and distribution in p55 mutant mice. Lymphocytes and endothelial cells from p55-deficient mice express normal levels of adhesion molecules considered important for lymphocyte migration to mucosal organs; this indicates that the lack of Peyer's patches does not result from a defect in lymphocyte homing. In summary, the p55 receptor for TNF selectively mediates organogenesis of Peyer's patches throughout ontogeny, suggesting that the effects of LT-alpha on the development of lymphoid organs may be mediated by distinct receptors, each functioning in an organ-specific context.

scholarly journals The histopathology of splenic lymphoma with villous lymphocytes

Blood ◽  
1994 ◽  
Vol 84 (11) ◽  
pp. 3828-3834 ◽  
Author(s):  
PG Isaacson ◽  
E Matutes ◽  
M Burke ◽  
D Catovsky
Keyword(s):  
Lymph Nodes ◽  
Marginal Zone ◽  
Molecular Characteristics ◽  
White Pulp ◽  
Splenic Marginal Zone Lymphoma ◽  
Mantle Zone ◽  
Marginal Zone B Cells ◽  
Splenic Lymphoma ◽  
Spleen And Lymph Nodes ◽  
Red Pulp

Whereas the hematologic, immunophenotypic, and molecular characteristics of splenic lymphoma with villous lymphocytes (SLVL) have been well documented, the histologic features of the spleen and lymph nodes remain uncharacterized. We have reviewed the histopathology of the spleen in 37 cases of SLVL and of involved splenic hilar lymph nodes in 6 cases. Tissue immunophenotyping was performed in 24 cases, 6 of which had frozen tissue available, and the results were compared with the membrane immunophenotype of the circulating villous lymphocytes and cells extracted from spleen and lymph nodes. In the spleen, SLVL is characterized by involvement of the white pulp follicles, which may be surrounded or replaced by the lymphoma cells. In the red pulp, the cells form small nodules and infiltrate diffusely with sinusoidal invasion. The cytologic appearance of the neoplastic cells varies from a resemblance to small mantle-zone--like lymphocytes to that of marginal-zone cells and there are scattered blast forms. In involved lymph nodes, the infiltrate again centers on the follicles that are usually replaced, but occasionally show preservation of follicle centers; sinuses are often preserved. The tissue immunophenotype is similar to that of marginal-zone B cells. Membrane immunophenotyping may give different results in some cases and may vary depending on the compartment from which the cells are obtained. SLVL in the peripheral blood is a histologically homogeneous entity identical to the condition previously characterised by histopathologists as splenic marginal-zone lymphoma.

VEGF and AMD3100-Induced Rapid Mobilization of C-Kit/Sca-1 Positive Murine Bone Marrow Cells and of Gr-1+/CD-11b+ Myeloid Cells Is Impaired in Urokinase (uPA) and Urokinase Receptor (uPAR) Deficient Mice.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 1384-1384
Author(s):  
Mohammad Dehghani ◽  
Damla Olcaydu ◽  
Pavel Uhrin ◽  
Bernd Binder ◽  
Johannes Breuss
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Ex Vivo ◽  
Myeloid Cells ◽  
Urokinase Receptor ◽  
Facs Analysis ◽  
Β1 Integrins ◽  
Deficient Mice ◽  
Marrow Cells

Abstract Hematopoietic Progenitor Cells (HPC) can be mobilized from bone marrow into the circulation in response to a number of stimuli including G-CSF, AMD3100 (antagonist of CXCR4-DSF-1 axis) and vascular endothelial growth factor (VEGF). The main mechanism for mobilization of HPCs upon stimulation by classical “mobilizers”as G-CSF is thought to be through extracellular matrix proteolysis in the marrow. Urokinase is a serine protease present in the marrow and contributes to mobilization of stem cells upon binding to its receptor (uPAR) and activating plasminogen that leads to matrix degradation. Our previous data show that the effect of VEGF on endothelial cell migration is exerted through activation of the uPA/uPAR system and through co-internalization of β 1 integrins. Upon internalization of these receptors, cells detach from their underlying extra-cellular matrix (ECM) as well as from stromal cells. We hypothesize that the contribution of VEGF to HPC mobilization occurs through a similar mechanism. We also want to analyze the influence of uPA/uPAR deficiencies on mobilization of Gr-1+/CD-11b+ myeloid and c-kit +/Sca-1+ (SK)cells by VEGF and AMD3100 and compare it with G-CSF as a classical “mobilizer”. Wild type, uPA knockout and uPAR knockout mice in C57BL6 background were used for in vivo experiments. We collected peripheral blood before and 2 hours after i.p. injection of VEGF-E and AMD3100 and assessed the number of SK cells and myeloid cells by FACS analysis. We also administered G-CSF for 5 days and compared blood samples before and after the experiment. To evaluate the effect of VEGF on HPC integrin expression, femurs of the respective animals were incubated with VEGF in an ex vivo experimental model and β1 expression was assessed by FACS analysis. In vivo data demonstrated a significantly reduced responsiveness of uPA−/− mice to VEGF-E in the first 2 hours after the injection. This decreased responsiveness to VEGFis observed in uPAR−/− mice but to a lesser degree than in uPA−/− mice..(40 +/−16 % and21 +/− 20% respectively vs 65 +/− 24 % in wt, means and SD). Injection of urokinase together with VEGF to uPA−/− mice rescues the lack of mobilization of SK cells. Ex vivo stimulation of uPAR knockout femoral bone marrow cells with VEGF for 20 minutes provides evidence that the internalization of β1 integrins upon VEGF stimulation is uPAR dependent. VEGF can also increase in vivo the number of Gr-1+/CD-11b+ myeloid cells after 2 hours in wt mice (96 +/− 45%) but not in urokinase deficient or urokinase receptor deficient mice (7 +/− 11% and 21+/−33%, respectively). AMD3100 has a strong effect on mobilization of SK cells in wt animals within 2 hours (increase of 2.8+/−0.78 times) but cannot mobilize these cells in uPA and uPAR deficient mice to the same extend (0.8+/−0.65 times and 0.1+/−0.07 respectively). G-CSF injection for 5 days mobilizes Gr-1+/CD-11b+and SK cells in wt and knock out mice to a similar extent, indicating that the capacity to release these cells from the bone marrow is not affected by uPA or uPAR gene deficiency. Our results demonstrate a reduced mobilization of uPA−/− and uPAR−/− HPCs and myeloid cells in response to VEGF compared to wt mice. VEGF leads to internalization of the expression of β1 integrins on the surface of SK cells in wt but not in uPAR−/− mice. In addition, we could show that the uPA/uPAR system plays a role in AMD3100-dependent mobilization of these cells. These data indicate that the uPA – uPAR system plays a pivotal role in short-term but not long-term bone marrow HPC and PMN leukocyte mobilization.

scholarly journals Lymphocytosis Induced in Mice by Supernatant Fluids of Bordetella pertussis Cultures: A Histopathological Study

Blood ◽  
1973 ◽  
Vol 42 (4) ◽  
pp. 611-621 ◽  
Author(s):  
Thomas J. Athanassiades ◽  
Stephen I. Morse
Keyword(s):  
Lymph Nodes ◽  
Bordetella Pertussis ◽  
Marked Decrease ◽  
Histopathological Study ◽  
White Pulp ◽  
Circulating Lymphocytes ◽  
Spleen And Lymph Nodes ◽  
Culture Supernatants ◽  
Lymphocyte Populations ◽  
Later Phase

Abstract Intravenous injection into mice of phase I Bordetella pertussis culture supernatants produces a marked lymphocytosis. The evolution of lymphocytosis was correlated with histopathological alterations in the lymphoid organs. The early phase, 17 hr to day 3, was associated with massive depletion of both lymphocytes from the white pulp of the spleen and of cortical thymocytes. There was a corresponding profound decrease of splenic and thymic weights. The later phase was associated with a marked decrease in lymphocytes of lymph nodes while concomitantly the spleen and thymus appeared to be repopulating. Both thymic-dependent and thymic-independent lymphocyte populations were mobilized from spleen and lymph nodes. There was a striking diminution in the number of lymphocytes contained within the walls of postcapillary venules (PCVS) of all lymph nodes between 2 and 7 days. The data suggest that initially the lymphocytosis is due predominantly to release of splenic lymphocytes and to a lesser extent of thymocytes into the circulation. Subsequently, the lymphocytosis is sustained by the depopulation of the lymph nodes. Lymph node depopulation is maintained by the failure of circulating lymphocytes to emigrate from the blood through the PCVS.

Sign in / Sign up

Export Citation Format

Share Document