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Biomedical subjects

C J Sanderson

Publications and source records attributed to C J Sanderson.

At least 19 recordsLinked to original sources
PubMed1992

Release of granule proteins from eosinophils cultured with IL-5.

Eosinophils isolated from normal individuals were cultured in the presence of human rIL-5 (hrIL-5) for up to 14 days, and the effects of this exposure were determined. First, the hrIL-5-cultured eosinophils were activated and degranulated more readily than freshly isolated eosinophils. For example, eosinophils cultured for 7 days with hrIL-5 released 30 and 10% of granule eosinophil-derived neurotoxin (EDN) when exposed to Sepharose 4B beads coupled to secretory IgA and IgG, respectively, whereas freshly isolated eosinophils released only 19 and 4%, respectively, of their EDN in response to the same stimuli. Degranulation of hrIL-5-cultured eosinophils was not augmented by further exposure to hrIL-5, whereas degranulation of freshly isolated cells to secretory IgA and IgG beads was increased by exposure to hrIL-5. Second, eosinophils cultured with hrIL-5 had prolonged viability in vitro. For example, after four days of culture with 50 U/ml of hrIL-5, 86% of eosinophils were viable compared to 12% in medium alone. Third, hrIL-5-cultured eosinophils became hypodense, and electron microscopy showed that they contained granules with core and matrix lucency and with evidence of granule fusion. Fourth, hrIL-5-cultured eosinophils spontaneously lost 30 to 60% of their EDN, eosinophil cationic protein, and eosinophil peroxidase and about 50% of their eosinophil granule major basic protein content compared to freshly isolated eosinophils, and all four of the granule proteins were released into the culture medium. Fifth, detailed studies of eosinophils cultured in hrIL-5 showed that 89 +/- 10% of the starting quantity of EDN could be recovered at 7 days. Whereas 99 +/- 1% of the EDN at day 0 was cell associated, by 7 days 60 +/- 9% was in the cell supernatants. Thus, hrIL-5 activates eosinophils, increases their viability, decreases their density, and their content of granule proteins and causes release of the granule proteins into culture fluids. The striking loss of granule proteins during culture with hrIL-5 may be an important mechanism for deposition of these cationic toxins in various diseases where IL-5 plays a role.

Blood Proteins↗
PubMed1992

Comparison of Nissen total and Lind partial transabdominal fundoplication in the treatment of gastro-oesophageal reflux.

Fifty-two patients with gastro-oesophageal reflux disease refractory to medical treatment were randomized to undergo a Nissen total (360 degrees wrap) or Lind partial (300 degrees wrap) transabdominal fundoplication. Each group was comparable in number (26 patients), mean age (47 and 48 years) and sex distribution (eight women). Preoperative and postoperative assessment involved a modified Visick score, 22-h intraoesophageal pH monitoring, endoscopy and manometry. Follow-up was at 6 weeks and between 3 and 33 (mean 13) months. The prevalence of heartburn and regurgitation and the results of pH monitoring improved significantly after both operations (P less than 0.001). At early assessment eight previously asymptomatic patients (31 per cent) from the Nissen group and six (23 per cent) from the Lind group experienced difficulty swallowing. Ten patients (38 per cent) in each group complained of 'gas bloat'. Both complications had improved at late assessment in the majority of patients. No statistically significant advantage could be demonstrated for either operation.

Adult↗
PubMed1992

Interactive effects of selenium, methionine, and dietary protein on survival, growth, and physiology in mallard ducklings.

Concentrations of over 100 ppm (100 mg/kg) selenium (Se) have been found in aquatic food chains associated with irrigation drainwater. Both quantity and composition of dietary protein for wild ducklings may vary in selenium-contaminated environments. Day-old mallard (Anas platyrhynchos) ducklings received one of the following diets containing 22% protein: unsupplemented (controls), 15 ppm Se (as selenomethionine), 60 ppm Se, methionine supplemented, 15 ppm Se with methionine supplement, or 60 ppm Se with methionine supplement. In a second concurrent experiment the above sequence was repeated with a protein-restricted (11%) but isocaloric diet. In a third concurrent experiment all ducklings received 44% protein with 0, 15, or 60 ppm Se added. After 4 weeks, blood and tissue samples were collected for biochemical and histological examination. With 22% protein and 60 ppm Se in the diet, duckling survival and growth was reduced and histopathological lesions of the liver occurred. Antagonistic interactive effects occurred between supplementary methionine and Se, including complete to partial alleviation of the following Se effects by methionine: mortality, hepatic lesions, and altered glutathione and thiol status. With 11% protein, growth of controls was less than that with 22% protein, Se (60 ppm) caused 100% mortality, and methionine supplementation, although protective afforded less protection than it did with 22% protein. With 44% protein, ducklings experienced physiological stress, and Se was more toxic than with methionine-supplemented 22% protein. These findings suggest the potential for antagonistic effects of Se, methionine, and protein on duckling survival and physiology.

Analysis of Variance↗
PubMed1992

Interactive effects of arsenate, selenium, and dietary protein on survival, growth, and physiology in mallard ducklings.

High concentrations of arsenic (As) and selenium (Se) have been found in aquatic food chains associated with irrigation drainwater. Total biomass of invertebrates, a major source of protein for wild ducklings, may vary in environments that are contaminated with selenium. Day-old mallard (Anas platyrhynchos) ducklings received an untreated diet (controls) containing 22% protein or diets containing 15 ppm Se (as selenomethionine), 60 ppm Se, 200 ppm As (as sodium arsenate), 15 ppm Se with 200 ppm As, or 60 ppm Se with 200 ppm As. In a concurrent experiment, the same sequence was repeated with a protein-restricted (7%) but isocaloric diet. After 4 weeks, blood and tissue samples were collected for biochemical and histological examination. With 22% protein and 60 ppm Se in the diet, duckling survival and growth was reduced and livers had histopathological lesions. Arsenic alone caused some reduction in growth. Antagonistic interactive effects occurred between As and Se, including complete to partial alleviation of the following Se effects: mortality, impaired growth, hepatic lesions and lipid peroxidation, and altered glutathione and thiol status. With 7% protein, survival and growth of controls was less than that with 22% protein, Se (60 ppm) caused 100% mortality, and As (200 ppm) caused mortality, decreased growth, and liver histopathology. These findings suggest the potential for antagonistic effects of Se and As on duckling survival, growth, and physiology with adequate dietary protein but more severe toxicological effects when dietary protein is diminished.

Animals↗
PubMed1992

Interleukin-5.

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Amino Acid Sequence↗
PubMed1991

Interleukin-5 enhances the in vitro adhesion of human eosinophils, but not neutrophils, in a leucocyte integrin (CD11/18)-dependent manner.

Interleukin (IL-5) was found to enhance the adhesion of eosinophils, but not neutrophils, to both microvascular and large vein endothelial cells in a dose-dependent manner. Granulocyte/macrophage-colony-stimulating factor (GM-CSF) and platelet-activating factor (PAF) enhanced both eosinophil and neutrophil adhesion. Significant increases in eosinophil CR3 expression, but not LFA-1, were observed following pre-incubation with PAF, IL-3, IL-5 or GM-CSF. Neutrophil CR3 expression was increased significantly by pre-incubation with PAF or GM-CSF, but not IL-3 or IL-5. Enhanced adhesion to human microvascular endothelial cells (HMVEC) or human umbilical vein endothelial cells (HUVEC) was inhibited by (ranked in order of potency) anti-CR3 alpha = common beta-chain greater than LFA-1 alpha. Anti-p150,95 alpha had no measurable effect. Basal expression of eosinophil CR3 with monoclonal antibody inhibited IL-5-induced eosinophil hyperadherence to HUVEC in a manner almost identical to inhibition in the presence of excess anti-CR3. Thus, a conformational or affinity change in adhesion receptors following activation seems more important than a simple increase in numbers. No inhibition of unstimulated eosinophil adhesion to HMVEC or HUVEC by CD11/18 monoclonal antibody was observed. These findings demonstrate that IL-5 enhances eosinophil, but not neutrophil, adherence reactions, by a mechanism dependent, at least in part, on the CD11/18 family of adhesion glycoproteins.

Antigens, CD↗
PubMed1979

The mechanism of K-cell (antibody-dependent) mediated cytotoxicity. III. The ultrastructure of K cell projections and their possible role in target cell killing.

The cytotoxic interaction between lymphoid K cells from normal rat spleen and antibody-coated P815 mastocytoma cells has been studied in conditions under which the number of cytolytic events occurring at the time of observation was at a maximum. Electron micrographs of material fixed during the first 15 min after contact between the target and effector cells had been initiated by centrifugation showed that the K cells produce long projections which push deeply into the P815 cells, causing infoldings of the plasma membrane and distortion of the nucleus. The plasma membranes of the effector and target cells, and the nuclear membrane, remain intact. Subsequently the target cells undergo violent cytoplasmic blebbing (zeiosis) which is the first stage of cell lysis. The evidence for the hypothesis that projections from lymphoid K cells develop as a result of contact between receptors on the K cell surface and antibody bound to the target cell, and that the projections are involved in the cytotoxic mechanism is discussed.

Animals↗
PubMed1979

A morphological study of the interaction between Trypanosoma cruzi and rat eosinophils, neutrophils and macrophages in vitro.

The interaction between trypomastigotes of T. cruzi and purified rat eosinophils, neutrophils and macrophages has been studied. Macrophages induced by dextran, became infected and the parasites multiplied as amastigotes, eventually being released as trypomastigotes into the medium. Eosinophils show an antibody-dependent phagocytosis, while neutrophil phagocytosis is enhanced by antibody. Electron microscopy showed that once inside the granulocyte phagosome, the trypomastigotes transform to amastigotes as a prelude to degeneration. This occurs as material apparently of granule origin accumulates in the phagosome. Eosinophils have the capacity to eject incompletely degenerated amastigotes into the medium. This phenomenon is discussed in relation to previous time-lapse cinematography studies of the lysis of chick erythrocytes by eosinophils, and reports that eosinophils release granule contents by means of a secretory vesicle.

Animals↗
PubMed1979

The mechanism of T-cell mediated cytotoxicity. VII. Lysis of isolated cytoplasts and karyoplasts.

Isolated P815 karyoplasts are up to four times more susceptible to lysis by T cells than intact cells, suggesting that the target cells nucleus or a nuclear associated structure may be particularly sensitive to cell-mediated cytotoxicity. Cytoplasts showed variable susceptibility. The morphological changes seen by time-lapse cinematography show that the first change seen with intact cells is a burst of zeiosis (membrane blebbing), whereas neither cytoplasts nor karyoplasts exhibit zeiosis. These observations suggest that zeiosis results from changes in the cytoskeletal system. This is discussed in relation to the possibility that T cells kill target cells by causing physical damage to a critical organelle inside the cell rather than to the membrane itself.

Animals↗
PubMed1979

The mechanism of T-cell mediated cytotoxicity. VI. T-cell projections and their role in target cell killing.

Electron micrographs of material fixed during the first 10 min of a T-cell cytotoxic system showed T-cell projections and T-cell burrowing into target cells. These observations were made possible by using a system with a very high rate of killing. The projections vary in shape and size, and can push deeply into the target cell, distorting organelles in their path, including the nucleus. The projections contain fine fibrillar material, to the exclusion of organelles. They push the target cell membrane in front of them to form pockets approximating to the shape of the projection. Areas of close contact occur between the projections and the target cell membrane, particularly at the leading edges. The likelihood that these projections develop as a result of contact with specific antigen, and are involved in the cytotoxic mechanism is discussed.

Animals↗
PubMed1978

Antibody dependent cell-mediated cytotoxicity of Trypanosoma cruzi: the release of tritium-labelled RNA, DNA and protein.

The cytotoxicity of normal rat spleen cells to antibody-coated Trypanosoma cruzi epimastigotes has been studied by assaying the release of [3H]-labelled macromolecules from the parasites. The release of thymidine (DNA) is slower than the release of uridine (RNA), suggesting that the nucleus is broken down more slowly than the cytoplasmic membrane. Less than 50% of the leucine (protein) is released when the parasites are lysed, whereas uridine (RNA) is almost totally released. In practical terms these results show that the release of incorporated radioisotope-labelled uridine can be used as a sensitive assay for cytotoxicity of T. cruzi. Cytotoxicity by normal rat spleen cells is antibody dependent and proportional to the logarithm of effector cell number. The lag phase and the rate of RNA release is not altered by centrifuging the parasites and effector cells to enhance contacts between them.

Animals↗
PubMed1978

A comparison of the cytotoxic activity of eosinophils and other cells by 51 chromium release and time lapse microcinematography.

Antibody dependent cytotoxicity of chicken erythrocytes by purified rat eosinophils, neutrophils, macrophages and K cells has been compared by 51Cr release and time lapse microcinematography. Techniques have been developed for purifying these effector cell types. Both eosinophils and neutrophils cause rapid release of 51Cr from erythrocytes. Time lapse observations indicated that this was the result of phagocytosis. Eosinophils show rapid membrane movement and repeatedly engulf and regurgitate the erythrocytes. On the other hand, neutrophils become quiescent after phagocytosing erythrocytes, and remain quiescent until the remains of the cell are expelled. Neutrophils presumably have a mechanism for the release of soluble material, as 51Cr is released rapidly. Macrophages show a similar quiescence after phagocytosis, but in these cells there is apparently no rapid mechanism to expel material, as there is no significant 51Cr release over 20 h. K cells appear to damage chicken erythrocytes more slowly than they destroy tumour cells. Mast cells cause antibody-independent cytotoxicity which can be attributed to the release of toxic materials. None of these effector cells produced the type of lysis seen with antibody and complement.

Animals↗