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Biomedical subjects

R B Sterzel

Publications and source records attributed to R B Sterzel.

At least 109 records · Page 6Linked to original sources
PubMed1983

A thymocyte-activating factor derived from glomerular mesangial cells.

The glomerular mesangium is centrally involved in immune-mediated glomerulonephritis. The mesangial cell is a mesenchyme-derived multipotential vascular pericyte, which shares several properties with macrophages. Cultured, proliferating rat mesangial cells produce a factor, mesangial cell-derived thymocyte-activating factor (MC-TAF), which physicochemically and biologically closely resembles macrophage interleukin 1. MC-TAF is heat labile, of low m.w. (approximately 15,000), and adheres to anion exchangers. MC-TAF acts to augment lectin-induced thymocyte proliferation and enhances peripheral lymphocyte production of interleukin 2. These findings suggest that a mesangial cell cytokine may interact with the cellular immune system in an antigenically nonspecific fashion to modulate immune responses in glomerular disease.

Animals↗
PubMed1983

Stimulation of rat mesangial cell proliferation by macrophage interleukin 1.

Conditioned media from LPS-activated rat peritoneal macrophages enhanced the proliferation rates of cultured rat glomerular mesangial cells. This macrophage-derived activity extensively co-purified with interleukin 1 (IL 1) activity through sequential ammonium sulfate precipitation, S-200 gel chromatography, DEAE-cellulose anion exchange chromatography, and phenyl-Sepharose chromatography. In addition, the macrophage-derived factor was heat-labile (80 degrees C) and inactivated by phenylglyoxal, thus allowing tentative identification as IL 1. Macrophage supernatants and purified IL 1 enhanced the proliferative rates of mesangial cells only in the presence of serum; the use of platelet-poor plasma or serum depleted of platelet-derived growth factor was without effect. IL 1 acted to increase the percentage of cycling cells, without a change in the length of the individual cell cycle times. These findings provide a potential mechanism whereby activated macrophages, in combination with platelet factors, enhance mesangial cell proliferation. Such processes may contribute to the mesangial hypercellularity frequently found in immune-mediated glomerulonephritis.

Animals↗
PubMed1982

Lysosomal enzymes in glomerular cells of the rat.

Whole isolated rat glomeruli (WG) were incubated with bacterial collagenase to separate epithelial cells (EC) from the cores of glomerular tufts (GC), which consisted of mesangial and endothelial cells, as demonstrated by electron microscopy. Lysates of WG, EC, and GC and of renal tubules were prepared by hypo-osmotic shock and freeze-thawing. Activities of the following acidic lysosomal hydrolases were measured: acid phosphatase, beta-glucuronidase, cathepsin-D, non-specific esterase, and aryl sulfatases A and B. The glomerular cell preparations showed activities of all studied enzymes. GC had higher activities than EC, save for nonspecific esterase. Studies of the recovery of acid phosphatase and beta-glucuronidase revealed that approximately 2/3 of the hydrolase activities present in WG was still measureable after collagenase treatment and that the bulk of this was found in the GC lysates. These findings demonstrate that the rat glomerulus and its cell components have considerable biochemical activities of acidic hydrolytic enzymes. These appear to be most prominent in the combined mesangial and endothelial cells of the GC components.

Acid Phosphatase↗
PubMed1982

Mesangial disposal of glomerular immune deposits in acute malarial glomerulonephritis of rats.

The disposal of immune complexes by the glomerulus and the participation of infiltrating monocytes were studied in acute malaria-associated glomerulonephritis. Young Sprague-Dawley rats were infected with Plasmodium berghei. Parasitemia reached a maximum after 8 to 12 days, ending by day 20. In all infected rats, renal immunofluorescence microscopy showed in all glomeruli granular deposition of rat IgG, IgM, and C3 in a mesangial distribution. The staining was strongest from days 8 to 12, then diminished and disappeared after day 32. By contrast, electron-dense deposits were rarely seen before day 16 when they became detectable in the mesangial matrix, particularly along the inner aspect of the glomerular basement membrane. They were most conspicuous on days 20 and 34 and disappeared by day 100. Few monocytes were detected in the glomeruli by electron microscopy and by histochemistry for nonspecific esterase. Highest counts of esterase-positive monocytes were found on day 10 (means 2.9 per glomerulus, range 0 to 5; normal control range 0 to 1). Total glomerular cell counts were transiently elevated on days 10 and 20. Renal functional damage of malarial rats was mild as reflected by a transient increase of urinary protein excretion, whereas serum urea values remained in the normal range. The results suggest that elimination of glomerular immune deposits in acute malarial glomerulonephritis of rats involves their gradual condensation and degradation in the mesangium which reduces detection by immunofluorescence while leading to formation of transient electron-dense deposits. In this model, the efficient disposal of glomerular immune deposits by the mesangium appears to minimize the infiltration of monocytes and to prevent aggravation of the glomerular injury.

Animals↗
PubMed1982

Renal localization of Tamm-horsfall protein in unilateral obstructive uropathy in rats.

The distribution of Tamm-horsfall protein (THP) within nephrons and in the renal interstitium of the kidney was examined in rats after unilateral ureteral ligation. Urinary casts containing THP were detected not only distal to the site of THP synthesis in cells of the ascending limbs of the loop of Henle, but also in more proximal portions of the nephron, suggesting retrograde intratubular movement of urine. THP-positive casts within Bowman's space of glomeruli were found by 6 hours and were maximal at 2 weeks after obstruction. At this time, THP was present in 25 per cent of all glomeruli, predominantly in central zones of the outer cortex. No morphologic evidence suggesting passage of THP across Bowman's capsule of these glomeruli was found. By contrast, interstitial THP aggregates resulting from urinary extravasation from tubules were detected throughout the study. These occurred earlier and were more numerous, albeit smaller, in the cortex where they were concentrated in periarterial and periglomerular sites. Multiple pathways for escape of urinary THP from tubules were demonstrated and included tubular ruptures and necrosis, forniceal tears, and venous polyps. Although occasional masses of THP in the interstitium were surrounded by inflammatory cells, the overall time course and distribution of interstitial THP deposits did not correlate closely with the development of widespread interstitial hypercellularity and scarring after obstruction. Although not directly linked to the pathogenesis of tissue injury in obstructive uropathy, THP provides an excellent marker of urinary extravasation and of the pathways of urine flow within the kidney under pathologic conditions.

Animals↗
PubMed1981

The cellular reaction in glomeruli of rats with anti-glomerular basement membrane nephritis.

This work examines the cellular reaction in glomeruli of rats with an acute form of anti-glomerular basement membrane (GBM) nephritis. After intravenous injection of rabbit-derived anti-GBM serum, heterologous and, later, autologous IgG fixed to the glomerular capillary loops. From day 1 to 11 of nephritis, glomerular hypercellularity was not appreciable or modest by qualitative histology, whereas morphometric evaluation revealed mild but significant increases of glomerular cell counts as compared to untreated controls. Histoautoradiographic studies of renal tissue 2 h after pulse administration of 3H-thymidine served to determine the proportion of glomerular cells which synthesized DNA, indicating forthcoming cell division. The mean labeling index (LI) of epithelial cells of Bowman's capsule was 1.8% in controls, rose 4- to 5-fold on the first day of nephritis and fell gradually from day 2 to 11. LI to tuft cells was 1.9% in controls, peaked on day 4, and fell thereafter. Histochemical staining for nonspecific esterase, a marker of monocytes and macrophages, revealed that glomeruli of normal rats contain very few stained cells (mean: 0.2/tuft section). In the course of nephritis, a gradual increase of esterase-positive cells took place in glomeruli which reached a plateau on day 4 (mean: 5.5/tuft section), indicating an influx of migrating monocytes. It is concluded that the injury of this model of anti-GBM nephritis involves markedly enhanced proliferation of intrinsic glomerular cells associated with infiltration of monocytes. Such a prominent cellular response is revealed by the applied quantitative methods in the absence of histologically impressive glomerular hypercellularity.

Animals↗
PubMed1981

Rat malarial glomerulonephritis. An experimental model of post-infectious glomerular injury.

This paper describes the immunopathologic findings in acute malaria-associated glomerulonephritis in the rat. Young Sprague-Dawley rats were infected with Plasmodium berghei berghei. The subsequent parasitemia and elevation of circulating Clq-reactive immune complexes were transient while the appearance of anti-plasmodial antibody in the serum was persistent. Sequential examination of renal tissue and urine revealed the following glomerular alterations: (a) granular, predominantly mesangial deposits of IgG, IgM, and C 3, (b) electron dense deposits in the mesangial matrix, (c) glomerular deposition of plasmodial antigen(s) and of anti-plasmodial antibody as demonstrated by acid elution studies, (d) hypercellularity of the glomerular tufts and (e) increased urinary excretion of high molecular weight proteins. All renal abnormalities were transitory, disappearing within one to three months. The results indicate that this form of acute malarial glomerulonephritis in rats is mediated by immune complexes involving plasmodial antigen. The disease resembles the transient glomerular injury complicating cases of Plasmodium falciparum infection in humans. As an easily reproducible model, rat malarial glomerulonephritis appears most suitable for further immunopathologic and functional studies of post-infectious glomerular disease.

Animals↗
PubMed1981

Complement does not facilitate plasmodial infections.

The influence of the complement (C) system on Plasmodial infections in vivo (Plasmodium berghei in rats) and in vitro (Plasmodium falciparum) has been determined. In rats C3 depletion by treatment of animals with the C3 inactivator isolated from cobra venom factor results in infection that develops more rapidly, reaches a higher peak of parasitemia and is associated with an increased mortality rate (60%), in contrast to a lower degree of parasitemia and lack of mortality in C3-intact rats. The infection of human red cells by P. falciparum is not affected when serum C is inactivated either by heat treatment or by incubation with preformed immune complexes. Furthermore, human sera genetically deficient in C2, C3, C4, or C5 are as effective in facilitating the infection of red cells as is C-intact serum. These data suggest that, in contrast to Babesia sp., the in vitro or the in vivo infection of red cells by Plasmodium sp is not facilitated by the availability of C.

Animals↗
PubMed1981

Glomerular podocyte cell junctions in nephrotic syndrome. I. Freeze-fracture studies in rat aminonucleoside nephrosis.

Aminonucleoside nephrosis was induced in rats after a single i.p. injection of puromycin aminonucleoside (PAN). Freeze-fracture studies of the glomeruli were done, three, six and ten days after PAN injection. The epithelial filtration slits disappeared six days after PAN injection. On the split plasma membrane of the podocytes three types of cell junctions which apparently were newly formed were seen: 1) single strands (occluding junctions of leaky type); 2) networks of limited extent, composed of strands and particles (maculae occludentes); 3) assemblies of particles or pits (maculae communicantes) connected by single strands. The cell junctions of podocytes were comparable with those found in human nephrotic syndrome. (Kühn et al., 1981).

Animals↗
PubMed1976

[Water and potassium metabolism changes].

The disturbances of water and electrolyte metabolism in the body can be subdivided into three large groups: 1) disturbances of free water which are related to the whole body water and are always coupled with changes in the osmolality of the internal environment and also of the interior of the cells (hypertension due to loss of water, hypotension in water intoxication); 2) isotonic changes of the volume of the extracellular fluid-oedema or extracellular dehydration. The latter are always coupled with a hypovolaemia and with a danger to the circulation which may end in shock. There is also a cumulative loss of potassium as a result of the dehydration reaction; 3) disturbances of the intracellular water metabolism which are associated with disturbances of the potassium metabolism. These may have grave consequences for the function of striated and smooth muscles, for the function of the nerves and various enzyme systems. Since the disorders of the extracellular water balance are generally best known, the attention is principally drawn in this paper to the hypertonic dehydration and the status of the potassium metabolism. The symptomatology of both conditions is discussed, and also their diagnosis with the simplest laboratory effort not associated with great loss of time (which is essential if valuable time is not to be lost before the laboratory results can be obtained). The theoretical considerations are supplemented with clinical examples and explanations of the treatment.

Adult↗
PubMed1976

[Disturbances of Free Water and Electrolyte Metabolism: Three large groups are differentiated].

1. Disturbances of free water which are related to the whole body water and are always coupled with changes in the osmolality of the internal environment and also of the interior of the cells. 2. Isotonic changes of the volume of the extracellular fluid- edema or extracellular dehydration. The latter is always coupled with a hypovolemia and with a danger to the circulation which may end in shock. There is also a cumulative loss of potassium as a result of the dehydration reaction. 3. Disturbances of the intracellular water metabolism which are associated with disturbances of the potassium metabolism. These may have consequences for the function of striated and smooth muscles, for the function of the nerves and various enzyme systems.

Adult↗