Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous work has demonstrated that in vivo hepatic macrophage complement receptor clearance function is depressed after thermal injury. To determine whether impairment of complement receptor function is important in host defense, the present study evaluated the effect of the depression of complement receptor function in uninjured animals on susceptibility to endotoxin shock and bacterial infection. Hepatic complement receptor clearance function was evaluated by measuring the hepatic uptake of a test dose (2.9 X 10(8)/100 g) of rat erythrocytes coated with anti-erythrocyte immunoglobulin M (EIgM) or EIgG in rats. Depression of hepatic complement receptor function was induced by the injection of EIgG. The hepatic uptake of the test dose of EIgM or EIgG was depressed after the injection of 8.7 X 10(8) EIgG per 100 g and 17.4 X 10(8) EIgG per 100 g but not after the injection of 2.9 X 10(8) EIgG per 100 g. This effect was shown not to be due to a decrease in hepatic blood flow or a depletion of serum C3 and was, therefore, due to a depression in hepatic macrophage complement receptor clearance function. Susceptibility to endotoxin shock was increased with the dose of 8.7 X 10(8) EIgG per 100 g, and susceptibility to infection with Pseudomonas aeruginosa was increased with the dose of 17.4 X 10(8) EIgG per 100 g. Therefore, depression of hepatic macrophage complement receptor clearance function with EIgG is associated with depressed host defense.
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PMID:Depressing hepatic macrophage complement receptor function causes increased susceptibility to endotoxemia and infection. 391 36

We previously demonstrated the suppression of cell-mediated immunity to Listeria monocytogenes by Pseudomonas aeruginosa-induced, macrophage-like cells. The present study was undertaken to evaluate the mechanism for this suppression. P. aeruginosa supernatant was shown to activate macrophages by the criteria of increased bactericidal capacities and increased attachment to glass surfaces. Acquired cellular resistance to L. monocytogenes could also be inhibited by macrophages from L. monocytogenes-pretreated mice. The depression of acquired immunity by P. aeruginosa- or L. monocytogenes-activated macrophages did not appear to be due to a reduction of antigenic stimulus after nonspecific macrophage activation. In contrast, our findings suggest that suppression is mediated by activated macrophages through a prostaglandin-dependent mechanism. In vivo administration of aspirin blocked the immunosuppressive effect of P. aeruginosa- or L. monocytogenes-activated cells. Moreover, the suppressive activity of supernatants of macrophages from Listeria-infected mice was reversed when indomethacin was present during supernatant generation. Finally, prostaglandin E1 treatment in vivo profoundly inhibited the induction of cell-mediated immunity to L. monocytogenes. The possible role and mechanism of prostaglandin in suppressing cellular immunity to intracellular bacteria are discussed.
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PMID:Suppression of cellular immunity to Listeria monocytogenes by activated macrophages: mediation by prostaglandins. 392 50

High doses of slime-extract from Pseudomonas aeruginosa was found to suppress the delayed type hypersensitivity response to sheep erythrocytes when administered intraperitoneally 1 to 3 days before or 3 days after intravenous sensitization of mice. Moreover, the spleen cells from sensitized and slime-extract treated mice transferred the depression to normal recipients. Inhibition of DTH response was also seen when recipients were injected with slime-extract 24 h before they were infused with spleen cells from donor mice immunized with sheep erythrocytes. The development of skin DTH was quantitated by footpad increase. The data suggest that slime-extract from P. aeruginosa induces in spleens of mice immunosuppressive cells which affect the immunization with sheep red blood cells.
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PMID:Depression by slime-extract from Pseudomonas aeruginosa of delayed type hypersensitivity to sheep erythrocytes. 393 54

Regulatory 5-DL-methyltryptophan (5-MT)-resistant mutants of facultative methylotrophic Pseudomonas sp. M. were obtained. They are able to excrete tryptophan into the growth medium (60 to 300 g/ml). 5-MTR regulatory mutants are characterized by depression of trpE, trpD and trpC genes, which causes the production of intermediates of tryptophan biosynthesis and results in trpA and trpB genes induction as well as in two-fold activation of N-5-phosphoribosyl anthranilateisomerase (trpF gene product). Besides, all mutants demonstrate reduction of synthase feed-back inhibition about 4-11-fold. Together with tryptophan excretion, 5-MTR regulatory mutants are able to excrete tyrosine and unable to utilize this amino acid as the sole carbon source, which points to multiple nature of the selective effect of 5-MT.
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PMID:[The tryptophan operon of the facultative methylotrophic bacteria Pseudomonas sp. M. III. Characteristics of regulatory 5-MTR mutants]. 395 24

To further delineate the mechanisms underlying murine pulmonary defenses against bacterial infection, we studied the effects of antioxidant enzymes and hydroxyl radical scavengers on pulmonary clearance processes. Intratracheal injection of catalase and superoxide dismutase resulted in prolonged intraalveolar residence of the enzymes, but caused no decrease in rates of clearance of either Staphylococcus aureus 502A or Pseudomonas aeruginosa PAO1. In contrast, dimethylsulfoxide and dimethylthiourea caused significant depression of clearance of P. aeruginosa without altering clearance of S. aureus. These results provide further differentiation between clearance processes affecting gram-negative and gram-positive bacteria and suggest that murine clearance of gram-negative organisms may be in part mediated by reactions which generate hydroxyl anion. In vivo administration of agents which inhibit hydrogen peroxide-, superoxide-, or hydroxyl anion-mediated reactions do not alter normal clearance of S. aureus.
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PMID:Modulation of pulmonary clearance of bacteria by antioxidants. 398 94

Analysis of bacteriophage CB3 infection of Pseudomonas aeruginosa strain PAT2 establishes that phage induced changes in net macromolecular synthesis are absent at nonpermissive phage growth temperatures (32 C). Alterations which are evident in the PAT2 strain at 37 C or in the fully permissive strain, PAO1C, at either warm or cold temperatures do not occur in PAT2 at low temperatures. CB3 DNA synthesis and the degradation of host DNA to approximately 78S components occur at 37 C, but are absent in PAT2 at 20 C. Nevertheless, attachment of phage DNA to host cytoplasmic material occurs under permissive and nonpermissive conditions. This binding of phage DNA at 20 C is identical in nature to phage DNA bound at 37 C. Thus, the conditional cold-sensitive PAT2 host function in the growth of CB3 is expressed subsequent to membrane binding of the infecting genomes but prior to the onset of the initiation of CB3 DNA synthesis, the inhibition of host DNA synthesis, and the transient depression in RNA synthesis which occurs in permissive cells.
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PMID:Cold-sensitive Pseudomonas RNA polymerase. I. Characterization of the host dependent cold-sensitive restriction of phage CB3. 420 17

High-pressure oxygen (HPO) therapy for Pseudomonas aeruginosa infections of burn wounds has not been as effective as in vitro studies predicted. Mitigation of HPO toxicity for P. aeruginosa by nutrients present at the burn site could explain the lack of in vivo success. Alternatively, HPO-induced depression of host defense mechanisms could negate beneficial effects arising from HPOs known toxicity for P. aeruginosa. Accordingly, mouse peritoneal exudate cells (PEC), preincubated for 24 h in 1 atm of air-CO(2), were used to study the in vitro effects of HPO or air-CO(2) on phagocytosis of P. aeruginosa or sheep erythrocytes (SRBC). Subsequent 2-h exposures of PEC to increasing numbers of bacteria, in an air-CO(2) atmosphere, decreased the percentage of bacteria cleared as well as PEC viability. Similar exposures of PEC to bacteria in an HPO atmosphere prevented the loss of PEC viability and increased bacterial clearance. In control experiments, increasing the number of SRBC relative to PEC decreased the percentage of SRBC cleared without decreasing PEC viability, as determined under air-CO(2); short (2 h) exposure to HPO did not affect SRBC clearance. Microscopic examination of PEC indicated that a 24-h preincubation in HPO decreased the percentage of PEC which could ingest SRBC during subsequent experimental exposures (2 h) to air-CO(2) or HPO. These data suggest that short periods of exposure to HPO promote the ability of PEC to clear pseudomonads by adversely affecting the bacteria. This in turn prevents a pseudomonad-induced depression of PEC viability and function. In contrast, prolonged HPO exposure may be detrimental to phagocytic activity.
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PMID:Inhibition of Pseudomonas aeruginosa by hyperbaric oxygen: interaction with mouse peritoneal exudate cells. 421 74

Endotoxin administered intravenously to a group of four calves resulted in disseminated intravascular coagulation. A sublethal dose of piromen, a commercially available Pseudomonas spp endotoxin, was used. Serial measurements of total plasma fibrinogen, soluble fibrin levels, ethanol gelation tests, protamine sulfate tests, fibrinogen-fibrin-related antigen (FR-antigen) and prothrombin and thrombin times were done.Initial depression of plasma fibrinogen with a nadir of about 40% of pre-endotoxin levels at eight to 11 hours post-endotoxin (+8 to +11 hours) followed by an overcompensation to 180% at +60 to +108 hours was shown. Soluble fibrin was demonstrated in plasma from +2 to +22 hours with a peak of 100-114 mg/100 ml at +4 to +9 hours. Positive plasma ethanol gelation and protamine sulfate tests, as well as the presence of serum FR-antigen, occurred consistently following endotoxin administration. Significant increases in prothrombin times (PT) from +4 to +40 hours and in thrombin times (TT) from +4 to +16 hours were demonstrated. The peak increase of PT at +8 to +10 hours was 180%. The peak increase of TT at +6 to +9 hours was 260-290%.
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PMID:Endotoxin induced disseminated intravascular coagulation in cattle. 427 65

Cephapirin sodium, a cephalosporin for parenteral use, was evaluated in vitro and in 27 patients. Cephapirin had activity equivalent to cephalothin against 25 strains each of Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, and Staphylococcus aureus; 10 strains each of Diplococcus pneumoniae, Pseudomonas species, and Enterobacter species; and 8 strains of Proteus species other than P. mirabilis. All strains of S. aureus and D. pneumoniae and most strains of E. coli, K. pneumoniae, and Proteus species were inhibited by concentrations of cephapirin achieved in the serum. Of 27 patients (20 with pneumonia, 2 with S. aureus empyema, and 5 with miscellaneous infections), 25 responded to cephapirin therapy. The only major toxicity thought to be drug-related occurred in a patient who developed reversible bone marrow depression with leukopenia, neutropenia, and anemia. Although cephapirin was painful on intramuscular injection, phlebitis and pain were absent in patients treated intravenously. In a controlled comparison of intravenously administered cephalothin and cephapirin in four additional patients, the latter caused much less pain than the former and caused no phlebitis.
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PMID:Clinical and in vitro evaluation of cephapirin, a new cephalosporin antibiotic. 459 41

The effect of splenectomy on the ability of alveolar macrophages of young and adult rats to phagocytize Pneumococci, Types 3 and 14, and Pseudomonas aeruginosa was studied. Young animals showed a significant (15%) decrease in the phagocytosis of pneumococci type 14, 4 weeks after splenectomy. This depression increased to 30% in 6 weeks' time. Such depression was also noted when young splenectomized rat alveolar macrophages were challenged with Pseudomonas aeruginosa but not with type 3 pneumococci 6 weeks postsplenectomy. Three months following splenectomy in young animals, the rats were grown and they seemed to regain their normal phagocytic activity against pneumococci type 14. Adult rats also showed no alteration in their phagocytic activity against type 3 pneumococci. Autoimplantation of the spleen had a protective effect on the phagocytosis of type 14 pneumococci, and a nonsignificant effect on that of type 3. The present study postulates a modulatory role of the spleen on alveolar macrophage function. Splenectomy may cause the impairment of local lower respiratory immune function, making lungs vulnerable to specific bacterial invasion. Such splenic modulatory effect on alveolar macrophage phagocytic function seems to be age and antigen specific.
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PMID:The effects of splenectomy and splenic implantation on alveolar macrophage function. 640 17


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