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At least 757 records · Page 42Linked to original sources
PubMed1987

Discrepancy in assessment of phagosome-lysosome fusion with two lysosomal markers in murine macrophages infected with Candida albicans.

Phagosome-lysosome fusion (P-LF) was studied in cultured mouse resident peritoneal macrophages after phagocytosis of Candida albicans. The macrophages were labeled with acridine orange (AO), the electronopaque colloidal Thorotrast, or both markers. After phagocytosis of heat-killed C. albicans, both markers were delivered to more than 95% of phagosomes. After ingestion of viable C. albicans by labeled cells, delivery of AO to phagosomes was highly suppressed (90%), and yet Thorotrast delivery was almost universal. After phagocytosis and 60 min of incubation, about 10 to 20% of the yeasts were killed, and a similar fraction of phagosomes was stained by the fluorescent marker. The evidence from Thorotrast transfer and assessment of yeast viability indicates that C. albicans largely resists intracellular killing by resident macrophages in the face of entirely uninhibited P-LF. We infer that AO must transfer to nearly all of the phagosomes but that it is evidently recognizable only in those in which the yeasts have been killed or possibly severely injured. This conclusion constitutes yet another limitation in the usefulness of AO for studying P-LF.

Acridine Orange↗
PubMed1965

Hypoferremia in mice and its application to the bioassay of endotoxin.

Baker, Phillip J. (University of Wisconsin, Madison), and J. B. Wilson. Hypoferremia in mice and its application to the bioassay of endotoxin. J. Bacteriol. 90:903-910. 1965.-The ability of endotoxin to induce hypoferremia in mice was used for the bioassay of endotoxin. A marked depression in the serum-iron levels of mice occurred 12 hr after the intraperitoneal injection of 0.01 to 100 mug of Escherichia coli endotoxin; similar results were obtained with 1.0 to 100 mug of Brucella abortus endotoxin. This biological response to endotoxin appeared to be specific, reproducible, and dose-dependent. As heat-killed cells of B. abortus and E. coli were also able to induce hypoferremia, this bioassay could be employed for the determination of the endotoxin content of killed-cell preparations. Treatment of endotoxin by acid hydrolysis, acetylation, or pyridine-formic acid greatly diminished the hypoferremic response as well as its lethality for mice. Pretreatment of mice with Thorotrast had little effect upon the ability of endotoxin to induce hypoferremia; however, a stimulation of the activity of the reticuloendothelial system (RES) by treatment of mice with triolein markedly reduced the ability of endotoxin to induce hypoferremia. The relationship between the hypoferremic response to endotoxin and alterations in the activity of the RES are discussed.

Animals↗
PubMed1967

Influence of thorotrast blockade and acute renal artery ligation on disappearance of staphylococcal enterotoxin B from blood.

The protein toxin staphylococcal enterotoxin B (SEB) produces a clinical syndrome somewhat similar to that of gram-negative endotoxins. Our studies indicate a further similarity to endotoxin in that SEB is rapidly cleared from the plasma of monkeys. However, data reported herein show that an effective Thorotrast blockade of the reticuloendothelial system (RES) does not produce a significant change in the rapid disappearance kinetics of SEB. This observation contrasts with what is known regarding endotoxin clearance. Furthermore, other data reported herein indicate that acute bilateral renal artery ligation produces a profound delay in SEB clearance from plasma. A possible mechanism for renal degradation of SEB is theorized. The RES may play a less important role in the clearance of SEB. This finding contrasts with the demonstrated importance of the RES in clearance and detoxification of gram-negative endotoxin.

Animals↗
PubMed1968

Cytoplasmic structures associated with an arbovirus infection: loci of viral ribonucleic acid synthesis.

Unique cytoplasmic structures, herein designated as type I cytopathic vacuoles (CPV-I), are found in chick embryo cells early in the logarithmic phase of Semliki Forest virus replication. High resolution autoradiography demonstrated that the CPV-I are loci of (3)H-uridine incorporation. This evidence correlates well with previous biochemical data and electron microscopy of the subcellular fractions active in Semliki Forest virus ribonucleic acid synthesis. Origin of the CPV-I within host cell cytoplasm is confirmed by the distribution of electron-dense tracer particles and sequential ultrastructural observations.

Animals↗