Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:6.3.5.5 (CPS)
 1,262 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanism for the infection-promoting effect of the capsular polysaccharide of Klebsiella pneumoniae (CPS-K) was investigated using the experimental system in which mice were infected intraperitoneally (i.p.) with a virulent strain of Salmonella enteritidis immediately after i.p. injection of CPS-K. In the peritoneal phagocytes of CPS-K-untreated control mice, approximately 70, 3, and 10% of phagocytized bacteria survived 6, 12, and 24 hr after challenge, respectively, when calculated from the ratio of the number of cell-associated viable bacteria, which was estimated by direct plate count, to the number of phagocytized bacteria, which was estimated by microscopic observation of stained smears. In contrast, almost all of the phagocytized bacteria were viable throughout the experimental period in mice treated with CPS-K. The electron microscopical findings of the phagocytes obtained 12 hr after challenge showed that in the cells of mice treated with CPS-K almost all of the phagocytized bacteria were morphologically intact, with some of them in the stages of cell division, whereas in those of untreated control mice, almost all of the phagocytized bacteria underwent digestive changes. When the reaction product of acid phosphatase was examined by electron microscopy in the phagocytes obtained 12 hr after challenge, the enzyme activity in the phagosomes was very low in mice treated with CPS-K in comparison with that in untreated control mice. Enzyme assays of the lysosomal and extralysosomal fractions of peritoneal cells obtained at various times after challenge also showed that release of acid phosphatase from the lysosomal fraction to the extralysosomal fraction after bacterial challenge was inhibited in peritoneal cells of mice treated with CPS-K.
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PMID:Effect of capsular polysaccharide of Klebsiella pneumoniae on host resistance to bacterial infections. III. Further study of its effects on interactions between peritoneal leukocytes and virulent Salmonella enteritidis. 38 55

1. A lag period of about 4 days preceded the onset of metamorphosis precociously induced by tri-iodothyronine in tadpoles of the giant American bullfrog (Rana catesbeiana). It was established by the accelerated synthesis or induction of carbamoyl phosphate synthetase and cytochrome oxidase in the liver, serum albumin and adult haemoglobin in the blood, acid phosphatase in the tail, and the increase in the hindleg/tail length ratio. 2. A 4- to 6-fold stimulation, 2 days after the induction of metamorphosis, of the rate of synthesis of rapidly labelled nuclear RNA in liver cells was followed by an increasing amount of RNA appearing in the cytoplasm. Most of the newly formed RNA on induction of metamorphosis was of the ribosomal type. An accelerated turnover at early stages of development preceded a net accumulation of RNA in the cytoplasm, with no change in the amount of DNA per liver. 3. Most hepatic ribosomes of the pre-metamorphic tadpoles were present as 78s monomers and 100s dimers; metamorphosis caused a shift towards larger polysomal aggregates with newly formed ribosomes that were relatively more tightly bound to membranes of the endoplasmic reticulum. 4. The appearance of new polyribosomes in the cytoplasm on induction of metamorphosis was co-ordinated in time with a stimulation of synthesis of phospholipids of the smooth and rough endoplasmic reticulum, followed by a gradual shift in preponderance from the smooth to the rough type of microsomal membranes. 5. Electron- and optical-microscopic examination of intact hepatocytes revealed a striking change in the distribution and nature of ribosomes and microsomal membranes during metamorphosis. 6. Ribosomes prepared from non-metamorphosing and metamorphosing animals were identical in their sedimentation coefficients and in the structural ribosomal proteins. The base composition and sedimentation coefficients of ribosomal RNA were also identical. Induction of metamorphosis also did not alter the incorporation of (32)P into the different phospholipid constituents of microsomal membranes. 7. Nascent (14)C-labelled protein with the highest specific activity was recovered in the ;heavy' rough membrane fraction of microsomes, whereas little (14)C was associated with ;free' polysomes. Protein synthesis in vivo was most markedly stimulated during metamorphosis in the tightly membrane-bound ribosomal fraction after the appearance of new ribosomes. 8. The rate of synthesis of macromolecules in vivo could not be followed beyond 7-8 days after induction because of variable shifts in precursor pools due to regression of larval tissues. 9. The stimulation of RNA and ribosome formation was specifically associated with the process of metamorphosis since no similar response to thyroid hormones occurred in those species (Axolotl and Necturus) in which the hormones failed to induce metamorphosis.
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PMID:The formation, distribution and function of ribosomes and microsomal membranes during induced amphibian metamorphosis. 558 18