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Biomedical subjects

P G Canonico

Publications and source records attributed to P G Canonico.

At least 19 recordsLinked to original sources
PubMed1977

Effects of pneumococcal infection on rat liver microsomal enzymes and lipogenesis by isolated hepatocytes.

Modification in the enzymatic complement and lipogenic functions of rat liver endoplasmic reticulum (ER) were shown to occur during pneumococcal sepsis. Glucose-6-phosphatase, 5'nucleotidase, esterase, and NADPH cytochrome C reductase decreased in activity by as much as 50% with respect to controls. Hydroxymethylglutaryl-CoA and NADH cytochrome C reductases were increased 6-and 2-fold, respectively. Alkaline phosphatase and inosine-5'-diphosphatase did not differ with respect to fasted controls. The lipogenic capacity of the ER was shown to be enhanced. In vitro [14C]acetate incorporation into cholesterol and other lipids by hepatocytes isolated from infected rats was increased 2-to 10-fold. It is concluded that the flow of acetyl-CoA in liver cell of Streptococcus pneumoniae-infected rats is toward lipogenesis rather than ketogenesis.

Animals↗
PubMed1977

Pathogenesis of respiratory Klebsiella pneumoniae infection in rats: bacteriological and histological findings and metabolic alterations.

Gram-negative bacterial pneumonias have been increasingly important as nosocomial infections. The following model was developed to study the pathogenesis and evaluate therapy of such infections. Intranasal instillation of rats with a suspension of 5 x 10(6) Klebsiella pneumoniae caused bronchopneumonia with 24 h. Bacteria were isolated from the lungs in large numbers (greater than 10(5) colony-forming units [CFU] for at least 13 days after inoculation. Thereafter, the viable concentration decreased to about 10(3) CFU at 21 days but increased to 10(4) CFU at 25 days. Mortality rarely exceeded 25%. Plasma zinc concentration decreased, and plasma seromucoid, lysozyme, and alpha2-macrofetoprotein increased during respiratory K. pneumoniae infection in rats. There seemed to be a linear relationship between seromucoid concentration and the concentration of K. pneumoniae in the lung expressed in log10 units. Plasma zinc, alpha2-macrofetoprtoein, or lysozyme levels, however, did not change until the concentration of bacteria retrieved fron lungs exceeded 4 to 5 logs, Analysis of blood samples obtained serially from the orbital sinuses revealed that rats that succumbed to infection had significantly higher levels of seromucoid, alpha2-macrofetoprotein, and lysozyme and lower levels of plasma zinc than infected rats that survived. Progressive increases in seromucoid and particularly in lysozyme and alpha2-macrofetoprotein appeared to be predicative of death. It is postulated that the threshold effect observed for alpha2-macrofetoprotein and lysozyme reflect significant damage to lung tissue, and thus these two variables are good indexes of the severity of this infection. We propose that this model may be of value in elucidating the pathogenesis of respiratory K. pneumoniae as well as in assessing various models of therapy.

Animals↗
PubMed1977

Fat of Coxiella burnetti in macrophages from immune guinea pigs.

The interaction between Coxiella burnetii and peritoneal macrophages obtained from immune guinea pigs was studied by transmission electron microscopy. Phagocytosis and subsequent fate of ingested phase I and II rickettsiae were compared. Phase I rickettsiae were more resistant to phagocytosis than were phase II organisms. Macrophages from phase I- and II-immunized animals were equally capable of phagocytizing rickettsiae. Phase I and II rickettsiae previously treated with normal serum multiplied and destroyed macrophages from guinea pigs that had been immunized with phase II rickettsiae. Phase II organisms were initially suppressed in macrophages from phase I-immunized animals, but eventually multiplied in these cells. In contrast, only phase I organisms were destroyed by macrophages from phase I-immunized animals. Treatment of rickettsiae with immune serum enhanced ingestion by macrophages and potentiated the destruction of organisms by both types of macrophages. The macrophage migration inhibition assay was performed on peritoneal exudate cells from immune animals. Migration of peritoneal macrophages from phase I-immunized guinea pigs was inhibited, whereas macrophages from phase II-immunized animals migrated when cells were cultured in the presence of killed, intact phase I or II C. burnetii.

Antibodies, Bacterial↗
PubMed1976

Electron microscopic study on the interaction between normal guinea pig peritoneal macrophages and Coxiella burnetii.

An electron microscopic study was conducted to explore the interaction between normal guinea pig peritoneal macrophages and phase I and II Coxeilla burnetii previously treated with either normal or immune serum. A comparison was made on the efficiency of phagocytosis and subsequent killing of rickettsiae by macrophages. Both phases of rickettsiae previously treated with normal serum multiplied within phagosomes after phagocytosis with resultant destruction of macrophages. In contrast, suspending rickettsiae in immune serum rendered them more susceptible to phagocytosis and potentiated their destruction within macrophages.

Animals↗
PubMed1976

Antibody response to Rocky Mountain spotted fever.

Various techniques were compared to determine the most sensitive method for detection of rocky Mountain spotted fever antibody. A radiometabolic technique for detection of Rocky Mountain spotted fever antibody is also described. In infected monkeys, the fluorescent antibody technique yielded the earliest evidence of seroconversion; with some monkeys the microagglutination procedure was equally effective. The fluorescent antibody and microagglutination measurements showed higher titers than those for complement fixation, Weil-Felix, or the radiometabolic techniques.

Agglutination Tests↗
PubMed1975

Phagocytosis of Francisella tularensis by Rhesus monkey peripheral leukocytes.

Phagocytosis of Francisella tularensis by rhesus monkey peripheral neutrophils (PMN, was assessed by autoradiography, electron microscopy, and biochemical techniques. PMN, in contrast to mononuclear phagocytes, were unable to phagocytize F. tularensis in vitro in the absence of immune serum. It is postulated that in the nonimmune host the innate inability of PMN to phagocytize F. tularensis deletes one of the possible mechanisms of host defense to bacterial infection and thus permits the early dissemination of F. tularensis to intracellular sites of specific target tissues.

Animals↗
PubMed1975

Temporal appearance of opsonizing antibody to Francisella tularensis: detection by a radiometabolic assay.

The burst in oxidative metabolism that is mediated through activation of the hexose monophosphate shunt and accompanies particle ingestion by polymorphonuclear leukocytes was used as the indicator in an in vitro radiometabolic assay for detection of specific opsonizing antibody to Francisella tularensis. Release of 14CO2 from radiolabeled glucose was increased significantly when specific immune serum added to suspensions of monkey polymorphonuclear leukocytes and F. tularensis. With this method, opsonizing antibodies to F. tularensis were detected in monkey serum 3 days after vaccination. Significantly increased opsonic activity in these monkeys preceded the appearance of, and persisted longer than, antibody activity as determined by conventional serological techniques. In addition, sera from 11 of 12 humans that were immunized 1 month to 13 years previously and had nondiagnostic agglutinating antibody titers demonstrated significant opsonizing activity.

Animals↗
PubMed1975

Relationship of serum beta-glucuronidase and lysozyme to pathogenesis of tularemia in immune and nonimmune rats.

A temporal study is reported of the febrile responses, tissue bacterial contents, and serum concentration of the lysosomal enzymes, beta-glucuronidase and lysozyme, in nonimmune rats inoculated with virulent or attenuated strains of Francisella tularensis, and in immune rats challenged with either a high or low dose of virulent organisms. The level of serum beta-glucuronidase appears to be an indicator of hepatocyte damage, whereas serum lysozyme correlates with the appearance, frequency, and severity of pyogranulomatous lesions. Survival of nonimmune rats after a challenge with either virulent or attenuated organisms appears to depend on a balance between dose of bacterial inoculum, celerity of irreversible pathologic events, and the ability of the reticuloendothelial and immune systems to collaboratively mount a response to limit or prevent dissemination of the infection. In immune rats, infection of parenchymal hepatic cells does not occur after a low dose (10-4) virulent challenge. Infection of parenchymal hepatic cells, however, does occur in immunized rats when the challenge dose is sufficiently large (10-8) so as to overcome the capacity of the reticuloendothelial to clear opsonized organisms.

Animals↗
PubMed1975

Characterization of monkey peripheral neutrophil granules during infection.

Rhesus monkey (Macaca mulatta) neutrophils were shown to contain the azurophilic granule maker enzymes myeloperoxidase and beta-glucuronidase but were deficient in the specific granule markers alkaline phosphatase (AKP) and lysozyme. Isopycnic centrifugation of leukocyte homogenates on linear sucrose gradients resulted in cosedimentation of myeloperoxidase and beta-glucuronidase with an equilibrium density of 1.18. After an intravenous inoculation of monkeys with Salmonella typhimurium AKP activity became marked, whereas that of beta-glucuronidase decreased and myeloperoxidase remained unchanged. Lysozyme was undetected throughout the course of the experiment, but was present in oil-induced peritoneal macrophages and peripheral mononuclear cells. The induced AKP exhibited partial latency and had an equilibrium density of 1.15. It is unclear, however, whether the induced AKP is associated with specific granules or cytoplasmic membranes. Hence, while these data are consistent with the presence of azurophilic granules in polymorphonuclear neutrophils from infected monkeys, the presence of specific granules in polymorphonuclear neutrophils of both uninfected and infected monkeys remains moot.

Alkaline Phosphatase↗
PubMed1975

Induced metabolic sequelae of tularemia in the rat: correlation with tissue damage.

Serum and liver zinc concentration, amino acid uptake by liver, seromucoid content, and alpha2-macrofetoprotein production were measured in vaccinated as well as nonimmune rats exposed to either virulent (SCHU S4) or attenuated (LVS) strains of Francisella tularensi. It appears that liver damage (pyogranulomatous lesions) must occur before there is any alteration in the above variables. The presence of bacteria in the liver is not of itself sufficient to lead to the onset of systemic, induced metabolic sequelae (IMS). The occurrence of zinc redistribution in all instances of increased serum protein synthesis may imply a necessary relationship between these two sequelae. Amino acid redistribution does not appear to be linked to serum protein synthesis. An endogenous mediator of systemic IMS can be detected in tularemic rats by injection of the serum of these animals into healthy recipients. The occurrence of zinc redistribution and increased serum protein synthesis in some groups of rats in the absence of amino acids uptake by liver, as well as the apparent differential dose responsiveness of these responses, are suggestive of a multiplicity of endogenous mediators.

Amino Acids↗
PubMed1975

Aminoisobutyric acid transport in primary cultures of normal adult rat hepatocytes.

In contrast to suspensions of freshly isolated hepatic parenchymal cells (HPC), short-term monolayer cultures of HPC displayed properties of active transport for the amino acid analog aminoisobutyric acid (AIB). The uptake of AIB was inhibited by KCN and iodoacetate, failed to occur at 4 degrees, and was stimulated by glucagon. The apparent Km for AIB uptake by cultured HPC was approximately 19 mM. Glucagon did not alter the apparent Km but did increase V.

Aminoisobutyric Acids↗
PubMed1975

Pathogenesis of tularemia in immune and nonimmune rats.

Pathogenesis of tularemia in nonimmune rats given (intraperitoneal inoculation) virulent strain (SCHU S4) or vaccinal strain (LVS) of Francisella tularensis and in immune rats given SCHU S4 is described. Both LVS and SCHU S4 caused pyogranulomas in liver and spleen of nonimmune rats. Nonimmune rats given 10(4) SCHU S4 organisms did not survive beyond 72 hours, but immune rats given challenge inoculum of 10(8) SCHU S4 organisms developed lesions and survived. Larger doses of LVS resulted in earlier onset of characteristic hepatitis and splenitis in nonimmune rats. Periportal lymphocytic infiltrates were present in the liver 48 hours after SCHU S4 challenge inoculation of immune rats and 96 hours after inoculation of LVS in nonimmune rats and were associated with intense macrophage aggregation. These changes indicate that the pathogenesis of tularemia is a result of the interdependency of the dose and virulence of the causative agent with the immune status of the host and that cellular immunity has a significant role in the response of the rat to tularemia.

Animals↗