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Query: UMLS:C0004623 (bacterial infection)
 15,226 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using a new in vitro method of measuring the chemotaxis of polymorphonuclear leukocytes from peripheral blood, a chemotactic index has been calculated. The mean chemotactic index of 320 in 24 patients with definite rheumatoid arthritis, was significantly less (P < 0.0005) than the mean of 555 in 24 normal controls matched for age and sex. The mean chemotactic index of 435 in eight patients with juvenile rheumatoid arthritis was also significantly less (P < 0.01) than that of 553 in similarly matched controls. The chemotactic index could not be correlated with age, sex, disease activity, drugs used in treatment, latex titer, immunoglobulin levels, or protein coating on the cells. However, there was a correlation between the chemotactic index and the serum complement B(1e)/B(1a) value (P < 0.01) in 17 patients with adult onset rheumatoid arthritis. Although the serum complement B(1e)/B(1a) values were within the normal range, the lowest chemotactic indices were associated with the lowest complement values. The chemotactic indices in three patients with severe connective tissue disease (seropositive rheumatoid arthritis, systemic lupus erythematosus, and polymyositis) returned to normal after 5 days' treatment with 60 mg of prednisolone per day. Incubation of the cells from patients with rheumatoid arthritis with hydrocortisone in vitro failed to alter the chemotactic indices. Prior incubation of normal cells with purified rheumatoid factor complexes, rheumatoid serum, or macromolecules of iron dextran impaired their chemotaxis. It is suggested that phagocytosis of complexes in vivo is a possible mechanism by which the chemotaxis of the polymorphonuclear leukocytes of patients with rheumatoid arthritis is impaired. This impairment in chemotaxis may explain the increased incidence of bacterial infection, both during life and as a cause of death in these patients.
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PMID:Chemotaxis of polymorphonuclear leukocytes from patients with rheumatoid arthritis. 515 8

Endogenous pyrogen/leukocyte endogenous mediator (EP/LEM) induces, in the host organism, a fever that is thought to be mediated to some extent via the production of prostaglandins. The role of prostaglandins in the EP/LEM-induced fall in plasma iron and zinc is less clear. To study this relationship, rabbits and rats were injected with an antipyretic dose of prostaglandin synthase inhibitors concurrent with heat-killed bacteria or endotoxin. These inhibitors, indomethacin and sodium salicylate, were successful in partially and totally blocking fever in rabbits and rats, respectively; however, they had no effect on the hypoferremia and hypozincemia of infection. We conclude that prostaglandins are probably not involved in the fall in plasma iron and zinc during acute bacterial infection. Further, since hypoferremia and hypozincemia occurred even though fever was blocked, the fall in trace metals due to infection is not dependent on the rise in both temperature.
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PMID:Relationship of trace metals to fever during infection: are prostaglandins involved? 633 45

The role of ceruloplasmin (ferroxidase I; EC 1.16.3.1) in iron metabolism during experimental Neisseria meningitidis infection was investigated. Plasma ceruloplasmin activity was found to increase greatly in mice during the convalescence phase of iron-controlled infection and after a plasma hypoferremia had occurred. Ceruloplasmin activity-deficient animals became hypoferremic as a result of an impaired release of iron from the reticuloendothelial system as shown by impaired return of reticuloendothelial system-processed heme iron in these mice. Hypoferremia in ceruloplasmin activity-deficient mice was associated with an increased resistance to N. meningitidis infection, an effect reversed readily by ceruloplasmin supplementation or iron addition. This evidence implicated ceruloplasmin activity as an important component in the regulation of the plasma transferrin iron pool and suggested that an important role of additional ceruloplasmin as an acute-phase protein might be related to the requirement of additional transferrin iron. This study also provided further evidence of the importance of transferrin iron and host hypoferremia in bacterial infection.
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PMID:Ceruloplasmin and regulation of transferrin iron during Neisseria meningitidis infection in mice. 642 41

Serious defects in the living conditions of the vast majority of people in the tropics, rather than racial factors, are the underlying reasons why anaemia is common, why malaria is rampant and why the complications of sickle cell disease are so serious. Mass illiteracy, poor environmental hygiene and widespread poverty with all their implications explain why malaria eradication programmes have so far failed in tropical Africa and why basic health-care schemes have been difficult to establish. Pregnant women are very vulnerable to the effects of anaemia, malaria and sickle cell disease. However, appropriate use of folic acid and iron supplements as well as malarial chemosuppression succeeds in maintaining haemoglobin concentrations at reasonable levels during pregnancy. If, for whatever reason, the haemoglobin level falls to under 4.4 g/dl or the haematocrit value is 0.14 or less, anaemia becomes an obstetric emergency. Both maternal and fetal mortality rise sharply, maternal death being due to anaemic heart failure, fulminating bacterial infection and shock from even small loss at delivery or abortion. With the haemoglobin concentration as low as 4.4 g/dl, blood transfusion greatly improves maternal but not necessarily fetal prognosis. Additional cause of morbidity in sickle cell disease is painful crises, the control of which remains largely unsatisfactory. Now that sickle cell disease can be diagnosed early in intrauterine life the idea of aborting the affected fetuses as a means of controlling or reducing sickle cell disease is well within the means of developed countries, but it is a line of approach which developing countries cannot afford at present.
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PMID:Anaemia, malaria and sickle cell disease. 675 46

The reactions to a number of histochemical stains by Michaelis-Gutmann (MG) bodies in 13 cases of malakoplakia are described. All MG bodies contained calcium and phosphate. Iron was present in six cases. Special stains failed to reveal the presence of micro-organisms. In six cases the MG bodies contained either lecithin or sphingomyelin and in three both phospholipids were present. There was no evidence of phospholipid of bacterial cell membrane derivation. Carbohydrate staining reactions suggested the presence of a neutral polysaccharide and an acidic non-sulphated polysaccharide (such as a sialoglycan). No histochemical evidence could be adduced to implicate bacterial cell membranes in the structure of the organic matrix of the MG body. The implications of these findings in the light of the association between clinical bacterial infection and malakoplakia are discussed.
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PMID:The histochemical features of the Michaelis-Gutmann body and a consideration of the pathophysiological mechanisms of its formation. 708 72

The authors study 14 different analytical parameters in the pleural fluid in order to recognize differential biological criteria, helping to establish an etiologic diagnosis in patients with suggestive clinical symptoms and biological data of an infectious process. In a group of 38 patients with bacterial exudative pleural effusion (22 of tuberculous origin and 16 secondary to non-specific bacterial infection), the following parameters were analyzed: total proteins, acid glucoprotein, X1, antytripsin, CDH, acid phosphatase, amylase, cholinest, copper, iron, pCO2, pO2 pH, glucose, and cholesterol. The results of amylase, copper, pCO2, pO2 and pH determinations in the pleural fluid show statistical significant differences between the tuberculous cases and the patients with non-specific infections. Lastly, the authors mention the minimal biological criteria necessary to confirm the tuberculous or non-specific bacterial etiology of a pleural fluid, stressing the value of the levels of cholinesterase, copper, pO2 and pH as differential data.
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PMID:[Tuberculous pleural effusion and pleural effusion secondary to non-specific bacterial infection: biochemical differential diagnosis (author's transl)]. 736 79

The cascade of physiologic mechanisms in response to infection, the acute-phase response, is recognized as playing a major role in host defence. One such response is the hypoferremia that is consistently reported to occur during bacterial infection. This study aimed to determine whether the alterations in plasma iron were conditionable using the conditioned taste aversion (CTA) paradigm. The regime involved the pairing of a novel-tasting saccharin solution with bacterial endotoxin. Seven days after the initial pairing of these stimuli (the test day), the saccharin solution was represented. Animals exposed to this condition displayed a significant reduction in the level of plasma iron. Animals treated with an intraperitoneal dose of 400 micrograms/Kg lipopolysaccharide (LPS) displayed lower conditioned iron levels than rats infused with 100 micrograms/Kg LPS; however, this difference was not significant. These results showed that in addition to other acute-phase responses (fever and anorexia), plasma iron alterations are able to be manipulated through behavioral manipulations.
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PMID:Behavioral conditioning of endotoxin-induced plasma iron alterations. 761 18

Synergistic inhibition of hematopoietic tumor growth can be observed in vitro when the iron chelator deferoxamine (DFO) is used in combination with an IgG mAb against the anti-transferrin receptor antibody (ATRA). Our goal was to ascertain whether similar findings could be seen in vivo. A high molecular weight conjugate of deferoxamine, known as hydroxyethyl starch (HES) DFO or HES-DFO, was tested in conjunction with C2, a well-defined rat antimouse transferrin receptor mAb, against the 38C13 tumor in C3H/HeN mice. It was shown that while neither HES-DFO alone nor C2 alone produced consistent, significant inhibition of tumor growth, the combination of HES-DFO and C2 produced virtually complete inhibition of initial tumor outgrowth. The latter combination failed, however, to inhibit the growth of established tumors. It was then found that when C2 was used in conjunction with RL34, another IgG ATRA, the two ATRAS were themselves capable of causing synergistic inhibition of the growth of 38C13 in vitro. When the two IgG ATRAS were used together in vivo, regressions of established tumors were observed. Moreover, the addition of HES-DFO to the IgG ATRA pair then caused more frequent regressions. Although there was never any obvious toxicity seen with a single IgG ATRA, the use of the IgG ATRA pair was associated with sporadic mortality. In addition, although HES-DFO by itself was also not associated with any obvious toxicity, combined treatment with HES-DFO and a single ATRA resulted in death due to bacterial infection in about half of the mice after 10-15 days. Combined treatment with HES-DFO and the ATRA pair resulted in death attributed to infection in nearly all of the mice after 6 days. Thus, an iron deprivation treatment protocol with HES-DFO and IgG ATRAS produced both a significant antitumor effect and an increased risk of infection in a murine model system.
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PMID:Inhibition of lymphoma growth in vivo by combined treatment with hydroxyethyl starch deferoxamine conjugate and IgG monoclonal antibodies against the transferrin receptor. 764 Nov 99

Polyclonal antibodies were prepared to purified breast milk lactoferrin and used in an ELISA to measure plasma concentrations in investigations of various aspects of the inflammatory response. They were also used, in situ, to evaluate granulocyte lactoferrin content in disease states. The first series of studies addressed the putative role of lactoferrin in the pathogenesis of the hypoferremic, hyperferritinemic response to acute inflammation. Dissociation between the lactoferrin response and the iron related changes in rheumatoid arthritis and after alpha-interferon administration suggested that the relationship observed in acute and chronic bacterial infection may reflect coincidental effects of inflammatory cytokines. That lactoferrin does not mediate the inflammatory hypoferremic response was established by the finding that bone marrow transplant recipients, post-myeloablation, developed a hypoferremic response during septic episodes despite virtually undetectable plasma lactoferrin concentrations. The second series of investigations employed the plasma lactoferrin concentration as an index of granulocyte activation and function in a number of inflammatory conditions. Markedly increased initial plasma concentrations in acute pneumonia reflecting profound intravascular granulocyte activation were documented to predict sepsis related mortality. Plasma and granulocyte lactoferrin studies established that viral infection is associated with an acquired granulocyte lactoferrin deficiency. Plasma measurements indicated that asthmatics, even when clinically asymptomatic, have evidence of persistent granulocyte activation.
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PMID:Lactoferrin and the inflammatory response. 776 25

Previous work has shown that the Pseudomonas-derived protease, pseudomonas elastase (PAE), can modify transferrin to form iron complexes capable of catalyzing the formation of hydroxyl radical (.OH) from neutrophil (PMN)-derived superoxide (.O2-) and hydrogen peroxide (H2O2). As the lung is a major site of Pseudomonas infection, the ability of these iron chelates to augment oxidant-mediated pulmonary artery endothelial cell injury via release of 51Cr from prelabeled cells was examined. Diferrictransferrin previously cleaved with PAE significantly enhanced porcine pulmonary artery endothelial cell monolayer injury from 2.3-6.3 to 15.8-17.0% of maximum, resulting from exposure to H2O2, products of the xanthine/xanthine oxidase reaction, or PMA-stimulated PMNs. Iron associated with transferrin appeared to be responsible for cell injury. Spin trapping and the formation of thiobarbituric acid-reactive 2-deoxyribose oxidation products demonstrated the production of .OH in this system. The addition of catalase, dimethyl thiourea, and the hydrophobic spin trap, alpha-phenyl-n-terbutyl-nitrone, offered significant protection from injury (27.8-58.2%). Since sites of Pseudomonas infection contain other proteases, the ability of porcine pancreatic elastase and trypsin to substitute for PAE was examined. Results were similar to those observed with PAE. We conclude .OH formation resulting from protease alteration of transferrin may serve as a mechanism of tissue injury at sites of bacterial infection and other processes characterized by increased proteolytic activity.
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PMID:Protease-cleaved iron-transferrin augments oxidant-mediated endothelial cell injury via hydroxyl radical formation. 776 95


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