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Biomedical subjects

C Tagesson

Publications and source records attributed to C Tagesson.

85 records · Page 5Linked to original sources
PubMed1976

Formation and inhibition of lysolecithin in human gallbladder bile.

Homogenized human gallbladder epithelium was incubated at 37 degrees C with 14C-lecithin in diluted gallbladder bile. During the incubation, lecithin was transformed to lysolecithin. The reaction rate was higher at pH 4.5 than at pH 7.0. No degradation of lecithin occurred if the reaction mixture did not contain the homogenate. Lysolecithin was mixed with red blood cells in (a) diluted human gallbladder bile and (b) 0.15 M saline. The surface activity in the different systems was then assessed from the amount of hemoglobin recovered in the red cell pellet after centrifugation. In human bile, 500 mug lysolecithin/ml did not affect the amount of hemoglobin recovered whereas in saline, concentrations exceeding 25-30 mug/ml affected the red blood cells such that no hemoglobin was pelleted by the centrifugation. Lysolecithin was further studied for effect upon lecithin-3H-cholesterol-dicetylphosphate liposomes containing 14C-glucose. The surface activity of lysolecithin was assessed from the distribution of 3H- and 14C-activity after centrifugation. Although 500 mug lysolecithin/ml increased the non-sedimented 14C-activity, 5000 mug lysolecithin/ml was necessary to decrease significantly the amount of sedimented 3H-activity. The results are interpreted such that phospholipase A activity from the gallbladder epithelium, if released into the gallbladder bile, may generate lysolecithin from lecithin. However, the surface activity and, thus, the inflammatory mediating activity of lysolecithin is inhibited by components in the gallbladder bile, possibly lecithin.

Bile↗
PubMed1976

The biochemical prerequisites for preventing pathogenic lysolecithin activity in the human gallbladder.

Human gallbladder epithelium was disintegrated to complete loss of microscopic structure and incubated at 37 degree C together with unlabelled lysolecithin and 14C-lysolecithin. During each incubation lysolecithin was degraded and stoichiometrically equivalent amounts of free fatty acids formed. The maximum rate of degradation was obtained at pH 7.0 and at 200 muM lysolecithin. With increasing amounts of gallbladder epithelial cell constituents the reaction became faster. After heating the epithelial components at 70 degrees C for 10 min the reaction was inhibited. The results suggest the presence of a heat labile lysophospholipase (phospholipase B) activity in the human gallbladder epithelium. This activity may operate to protect the gallbladder epithelium against potentially pathogenic lysolecithin activity. Its presence in the gallbladder epithelium meets the prerequisites for a local anti-inflammatory mechanism and lends further support to the hypothesis of lysolecithin as a mediator of cholecystitis.

Cholecystitis↗
PubMed1975

On the physical-chemical effect of colostral antibody binding to Escherichia coli O 86.

Sensitization of Escherichia coli O 86 with colostrum or purified colostral sIgA antibody produces a physical-chemical change of the bacterial surface detectable as a change in partition in dextran-polyethylene glycol polymer two-phase systems. Sensitization with colostrum or sIgA reduces affinity for the dextran-rich phase. In contrast immune serum, IgG and complement increase the affinity for that phase. The results are compatible with the hypothesis that hydrophilic particles, e.g. certain strains of bacteria, are less liable to attachment to and phagocytosis by animal cells than hydrophobic particles, e.g. other bacterial strains. Sensitization with secretory IgA enhances the hydrophilicity thereby making possible an escape mechanism operating at the mucosal surfaces.

ABO Blood-Group System↗
PubMed1975

The prerequisites for local lysolecithin formation in the human gallbladder.

Human gallbladder epithelium was disintegrated to complete loss of microscopic structure. The material obtained - an extract - was incubated at 37 degrees C together with a mixture of lecithin and lysolecithin, phospholipids known to be present in bile. During such incubation a change in the phospholipid composition occurred, indicating that lecithin was converted to lysolechitin. This conversion increased in the presence of CaCl2. Heating the disintegrated epithelium (70 degrees C for 10 min at pH 4) considerably increased the phospholipid conversion. The results are consistent with the presence of phospholipase A activity in human gallbladder epithelium. The possible significance of this activity is discussed in view of the inflammation-mediating activity of lysolecithin in the gallbladder epithelium.

Calcium Chloride↗
PubMed1975

Lysolecithin-mediated inflammatory reaction in rabbit gallbladder. Permeability increase and enzyme liberation.

Aseptic inflammation in the gallbladder wall was studied in vitro using rabbit gallbladders. Wall permeability changes, measured as changes in the transmural passage of radioactively labelled hippuran and biligraphin as well as enzyme (acid phosphatase) release from wall to lumen were registered as parameters permitting quantitative assessment of an inflammatory process. Lysolecithin, a surface-active substance of possible significance in the pathogenesis of acute cholecystitis was chosen as inflammation-inducing agent. When 6-20 mg/ml lysolecithin was instilled into the gallbladders, dose-dependent increases in permeability and enzyme release occurred. No effects as compared with controls were seen when 2 mg/ml was instilled. Lysolecithin-treated gallbladders showed morphological signs of inflammation as opposed to untreated. The data reported are consistent with earlier observations that lysolecithin may cause inflammatory lesions to the gallbladder wall. The experimental model used may prove useful in examining the effects of aggressive and protective agents upon the gallbladder mucous membrane.

Acid Phosphatase↗
PubMed1974

Influence of hyperimmune immunoglobulin G on the physicochemical properties of the surface of Salmonella typhimurium 395 MS in relation to interaction with phagocytic cells.

Partition in an aqueous, two-polymer phase system containing dextran and polyethylene glycol was employed to investigate the physicochemical changes inflicted by the presence of immunoglobulin G (IgG) antibodies on the cell surface of a smooth strain of Salmonella typhimurium. Adding increasing amounts of anti-Salmonella IgG to the bacteria decreased the affinity for the polyethylene glycol-rich top phase, with a concomitant increase in in vivo clearance and in vitro phagocytosis by rabbit polymorphonuclear cells. Similarly, S --> R mutations in the same S. typhimurium strain decrease the affinity for the top phase and increase the liability to phagocytosis. The limiting antibody concentration to demonstrate increase of in vitro phagocytosis was approximately the same as that to produce a significant effect in the phase system, whereas lower concentrations were needed to increase the in vivo clearance. The results show that adsorption of IgG antibodies to bacteria brings about physicochemical changes of the cell surface which seem to promote the phagocytosis by polymorphonuclear cells and uptake in the reticuloendothelial system.

Animals↗
PubMed1973

Characterization of mutants of Salmonella typhimurium by counter-current distribution in an aqueous two-polymer phase system.

An aqueous, two-polymer phase system was employed in an attempt to separate and characterize a series of R mutants, derived from Salmonella typhimurium 395 MS, with differing lengths of lipopolysaccharide chains on their surfaces. R mutants with varying degrees of virulence and phagocytic resistance were unresolved in this system. However, the smooth MS bacteria were clearly separated from the rough cells and showed a high affinity for the polyethylene glycol-rich top phase. A uridine 5'-diphosphate-gal-4-epimeraseless mutant, phenotypically in R or S form depending on the growth medium, partitioned as the R mutants and S bacteria, respectively. These results demonstrate the great influence of long polysaccharide chains on the physicochemical properties of the cell surface.

Bacteriological Techniques↗
PubMed1973

Partition of Salmonella typhimurium in a two-polymer acqueous phase system in relation to liability to phagocytosis.

Analysis of the partition in a two-polymer phase system of Salmonella typhimurium R mutants with different susceptibility to phagocytosis distinguished between the mutants. Close to 80% of the R mutants least resistant to phagocytosis accumulated in the dextran-rich phase, whereas more phagocytosis-resistant mutants showed higher affinity for the interface and the polyethylene glycol-rich top phase. By growing the uridine diphosphate (pyro)-gal-4-epimeraseless mutant LT2-M1 in the presence of d-galactose for different periods of time, two well-defined peaks were obtained in counter-current distribution analysis with an aqueous two-polymer phase system revealing a heterogeneous population in the culture. One peak was located at a site characteristic of R bacteria, the other at the site of S bacteria. As growth proceeded, more bacteria transferred from the R-type to the S-type peak. Within each peak, a gradual increase in resistance to phagocytosis by rabbit polymorphonuclear cells occurred with increasing length of growth in d-galactose.

Countercurrent Distribution↗
PubMedDate not supplied

Calcium ionophore-activated neutrophils prestimulated with endotoxin increase pulmonary arterial pressure and vascular leakage in isolated perfused rat lungs: role of platelet-activating factor.

The influence of stimulated polymorphonuclear neutrophils on pulmonary arterial pressure and vascular leakage in isolated perfused rat lungs was investigated. We exposed isolated neutrophils to various stimuli in vitro, instilled the cells in the lung perfusate, and studied the effects on pulmonary arterial pressure and passage of fluorescently labeled dextran (4100 dalton) from the pulmonary circulation into the lung. We found that neutrophils stimulated with the calcium ionophore A23187 or with E. coli endotoxin had no significant influence on the pressure or the passage of dextran. On the other hand, neutrophils preincubated with endotoxin and then stimulated with A23187 caused significant increases, both in pulmonary arterial pressure and accumulation of dextran in the lung. Both these effects were attenuated by BN 52021, a specific platelet-activating factor antagonist, and by nordihydroguaiaretic acid, an agent that inhibited the generation of platelet-activating factor in A23187-stimulated neutrophils. These findings demonstrate that activated neutrophils can increase pulmonary arterial pressure and lung fluid accumulation and suggest that endotoxin-stimulated activated neutrophils exert at least some of their action via generation of platelet-activating factor.

Animals↗