Splenic Reticuloendothelial Cells Research Articles

Humoral proinflammatory cytokine and SAA generation profiles and spatio-temporal relationship between SAA and lysosomal cathepsin B and D in murine splenic monocytoid cells during AA amyloidosis.

Evidence shows that tissue macrophages (MPhis), in mice undergoing AA amyloidosis, endocytose acute-phase humoral serum amyloid A (SAA) and traffic it to lysosomes where it is degraded. Incomplete degradation of SAA leads to intracellular nascent AA fibril formation. In vitro, cathepsin (Cat) B is known to generate amyloidogenic SAA derivatives, whereas Cat D generates non-amyloidogenic SAA derivatives, and interferon (IFN-gamma)-treated MPhis show selective increase in Cat B concentration, a factor conducive to AA amyloidogenesis. To understand the cumulative effect of these factors in AA amyloidosis, humoral levels of SAA, IFN-gamma, tumour necrosis factor (TNF-alpha) and granulocyte-macrophage colony-stimulating factor were determined in azocasein (AZC)-treated CD-1 mice. We correlated these responses with the spatio-temporal distribution of SAA, Cat B- and Cat D-immunoreactive splenic reticuloendothelial (RE) cells. AZC-treated CD-1 mice similar to that of A/J mice showed partial amyloid resistance; their peak humoral IFN-gamma and SAA responses overlapped during the pre-amyloid phase. Unexpectedly, Cat D immunoreactivity (IR), instead of Cat B IR, was predominant in the splenic RE cells, indicating an apparent lack of causal relationship between IFN-gamma-mediated increase in Cat B expression. Partial amyloid resistance in CD-1 mice, probably a genetic trait, may be linked to high levels of Cat D expression, causing a delay in nascent AA fibril formation.

Immunolocalization of lipid peroxidation/advanced glycation end products in amyloid A amyloidosis

Chronic inflammation, superimposed by amyloid fibril deposition, is believed to trigger the cascade of oxidative stress response in the affected organs and tissues. We examined immunohistochemically the distribution of 4-hydroxy-2-nonenal (HNE) and N ε-(carboxymethyl)lysine (CML), markers of lipid peroxidation and advance glycation end products (AGE), respectively, in spleen sections and peritoneal macrophages (MΦ) from mice before and during AA amyloidosis. With time, both HNE and CML immunoreactivities increased significantly in MΦ and splenic reticuloendothelial cells, known to be associated with the clearance of serum amyloid A, the precursor of AA fibrils. HNE and CML were localized to the plasma membrane and the cytoplasmic compartment of MΦ and HNE only at the nuclear membrane. These markers were also colocalized bound to AA fibrils infiltrating the splenic sinus walls. Our results reinforce the notion that oxidative stress is an integral component of amyloidotic tissues. Both lipid peroxidation and AGE have been implicated in protein modification and amyloid fibril formation. The significance of HNE and CML associated with the monocytoid cells and implicated in SAA clearance and AA fibril formation, is discussed with the pathogenesis of AA fibrils.

犬ジステンパーにより死亡したと考えられた野生狸の1例

A dead wild racoon dog was examined pathologically. Grossly hepatization of the lungs was seen. Histologically, eosinophilic cytoplasmic inclusion bodies were found in the cytoplasm of splenic reticuloendothelial cells, surface epithelial cells of the stomach, transitional epithelial cells of the bladder, and the bronchiolar epithelial cells. Electron microscopically, crystalline-arrayed nucleocapsids were observed in the splenic reticuloendothelial cells and transitional epithelial cells of the bladder. From these findings, the death of the racoon dog may be attributed to the growth of canine distemper virus in cells of the lungs, spleen, stomach, bladder and bronchia.

Papovavirus Infection in Hand-Fed Parrots: Virus Isolation and Pathology

Papovavirus infection was diagnosed in 44 parrots of at least 18 species exclusive of the budgerigar (Melopsittacus undulatus). The birds were 14 days to 4 months old and had been removed from parental care and hand-fed as nestlings. The birds had been unexpectedly found dead after having evidenced no premonitory signs of illness, or they died following a short (12-to-48-hour) period of lassitude and anorexia. In most cases, necropsies revealed pallor, multiple hemorrhages, splenomegaly, and hepatomegaly with multifocal necrosis. Histological lesions included multifocal to diffuse hepatic necrosis that spared the periportal hepatocytes, karyomegaly of splenic reticuloendothelial cells and cells in other tissues, membranous glomerulopathy, and necrosis of bursal medullary lymphocytes. Papovaviruses were isolated from two cases, and papovavirus infection was confirmed in 27 of the birds by the fluorescent-antibody test using a conjugate against a papovavirus isolated from a budgerigar.

An electron microscopical and histochemical study on ferric nitrilotriacetate-induced "F1 amyloidosis".

Of a total of 80 offspring obtained by reciprocal crossing of ICR/JCL strain of mice of both sexes receiving 84-140 injections of Fe-NTA over 98-163 days before crossing, 52 (65%) showed severe generalized amyloidosis after 93-502 injections of Fe-NTA over 115-522 days, but not "hemochromatosis", which was a striking contrast to the findings of "hemochromatosis" without amyloidosis observed in the parent mice. Electron microscopic examinations revealed numerous bundles of non-branching, well-oriented amyloid fibrils radiated outward from the surface of cytoplasmic invaginations of the Kupffer cells or splenic reticuloendothelial cells of the F1 mice with amyloidosis, and close contact frequently observed between "amyloid-forming cells" and adjacent lymphocytes in the amyloid-laden liver and spleen of the F1 mice. Since the above findings in the F1 mice were not found in the parent mice treated with multiple Fe-NTA injections, the present authors assumed that the immunological memory for the Fe-NTA conjugate transmitted via the placenta to the fetus from the mother that received multiple Fe-NTA injections might be involved in the development of generalized amyloidosis in the F1 mice, although the possible mechanism by which Fe-NTA-induced "F1 amyloidosis" has been developed remains yet undetermined.

Major histocompatibility complex-linked spleen-dependent transfusion "collapse curves" in inbred rats.

In most donor-host combinations among seven inbred rat strains, transfused allogeneic red blood cells were cleared from the circulation of unsensitized hosts at a rate no different from that of syngeneic red blood cells. In four strain combinations, however, allogeneic red blood cells were cleared very rapidly, and in six combination, clearance was effected at a rate intermediate between the rapid clearance rate and the syngeneic rate. In strain combinations exhibiting rapid clearance, females cleared allogeneic red blood cells significantly more rapidly than did males. Rapid clearance was linked to the major histocompatibility complex (MHC) of the donor strain but not to the MHC of the host strain. All donor-host combinations showing rapid clearance possessed identical RT2, RT3, and AgS red blood cell alloantigens. Red blood cells removed rapidly from the circulation by allogeneic hosts were sequestered in the spleen rather than lysed in the circulation. The phenomenon was mediated by splenic reticuloendothelial cells and could be completely circumvented by prior splenectomy. Rapid clearance was apparently not antibody mediated. The phenomenon of rapid clearance of allogeneic red blood cells in rats appears to be analogous to the "collapse curves" of human blood transfusion.

Histochemical study of Hurler's disease by the use of peroxidase-labelled lectins.

Peroxidase-labelled lectins specific for various carbohydrate residues were used as histochemical reagents in the investigation of Hurler's syndrome. Peanut lectin was used to detect terminal D-galactose, wheatgerm lectin for N-acetyl-D-glucosamine, soybean lectin for N-acetyl-D-galactosamine, Tetragonolobus lotus lectin for alpha-L-fucose and Bandeiraea S. lectin for alpha-D-galactose. It was found that Kupffer cells in the liver and splenic reticulo-endothelial cells contain acid mucopolysaccharides which bind lectins in paraffin sections after appropriate fixation. The pattern of lectin binding suggests that such cells contain significant amounts of D-galactose, L-fucose, N-acetyl-D-galactosamine and N-acetyl-D-glucosamine. It is likely that the last named carbohydrate is present as a polymer. Neurones contain a different carbohydrate, rich in galactose and fucose but poor in N-acetyl-D-glucosamine. This compound is resident to lipid extraction. Hepatocytes, as a rule, do not react with lectins, most likely because of loss of the more soluble mucopolysaccharides during fixation. The results are consistent with the biochemical data of Hurler's syndrome and indicate that lectins can be a useful tool for the investigation of the cytochemistry of storage disorders.

The effect of partial splenectomy on experimental pneumonoccal bacteremia in an animal model

The effect of total and partial splenectomy on the blood stream clearance of type 23B Streptococcus pneumoniae was studied in chinchillas 2 wk and 2 mo following surgery to determine the amount of splenic tissue necessary for protection against overwhelming sepsis. Significantly more pneumococci were found in the blood of totally splenectomized chinchillas than in the blood of sham-operated animals throughout the 6-hr sampling period after intravenous inoculation of pneumococci. Animals that had two-thirds of their spleen removed demonstrated a significant delay in clearance of pneumococci compared with sham-operated and hemisplenectomized animals. The rate of pneumococcal clearance was similar for the sham-operated and the hemisplenectomized group, and was significantly prolonged but similar among totally splenectomized and two-thirds splenectomized animals. Pneumococcal opsonic activity was reduced only in the sera of totally splenectomized chinchillas 2 mo after surgery. There was no positive relationship between pneumococcal clearance and change in pneumococcal opsonic activity. These results suggest that the impaired clearance of circulating pneumococci in splenectomized animals is due to the loss of splenic reticuloendothelial cells as a mechanical filter, rather than deficient serum opsonic activity. There appears to be a critical splenic mass required for optimal bacterial clearance, and hemisplenectomy may protect against overwhelming postsplenectomy sepsis.

Causes and Temporal Sequence of Onset of Functional Asplenia in Adults

To determine the causes and time course of onset of functional asplenia in adults, a four-part investigation was conducted. This consisted of a review of the world's literature, a survey of colleagues, a detailed study of 4,476 consecutive liver-spleen scans in three hospitals, and continued monitoring of 3,500 scans in five hospitals. Based on the findings, a classification was proposed of the causes of functional asplenia. The two major etiologies were circulatory disturbances and effects directly on splenic reticuloendothelial cells. The time course varied from the essentially instantaneous onset of functional asplenia in patients with acute splenic artery obstruction, to a prolonged and gradual onset in those with chronic damage to splenic reticuloendothelial cells. Functional asplenia was found in 0.14% of the adults who had liver-spleen scans for other indications.

Marble Spleen Disease in Ring-Necked Pheasants: Histology and Ultrastructure

Marble spleen disease in pen-raised ring-necked pheasants runs a peracute course, with death occurring from pulmonary edema. The diagnosis can be made from the gross and microscopic lesions. Large eosinophilic to pale basophilic inclusion bodies were consistently present in splenic reticuloendothelial cells. A smaller and less numerous basophilic intranuclear inclusion body also occurred in tEe spleen and lungs. The presence of amyloid in the spleen was established by electron microscopy and histochemical stains. A viral etiology was postulated from electron microscopic evidence demonstrating numerous spherical virus particles in the splenic intranuclear inclusions. Attempts at virus isolation by inoculation of three avian tissue culture systems with infected spleen were unsuccessful.