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)

Tumor necrosis factor, lymphocyte-activating factor, and enhanced levels of type I interferon were found in serum samples taken 2 h after mice infected with Plasmodium vinckei subsp. petteri received a small intravenous injection of endotoxin. These three mediators are among those released when mice receive an endotoxin injection 2 weeks after Mycobacterium bovis BCG or Corynebacterium parvum have been administered. There is indirect evidence that this wider range of mediators is also released in P. vinckei subsp. petteri-infected mice given parenteral endotoxin. A recent report that endotoxin is detectable in the plasma of malaria-infected mice and children implies that these mediators may also be released in the acute phase of the natural infection. We propose that these macrophage-derived mediators may be important in the glucocorticoid antagonism, bone marrow depression, fever, hypergammaglobulinemia, splenomegaly, elevation of serum amyloid A, consumptive coagulopathy, and shock syndrome with associated organ damage which can accompany malaria. The intraerythrocytic parasite death seen at crisis in some malarias, as well as the subsequent development of specific protective immunity, may also depend on these mediators.
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PMID:Possible importance of macrophage-derived mediators in acute malaria. 616 64

Induction of gamma (Type II) interferon results in depression of the cytochrome P-450 system of mice. The gamma interferon is induced by sensitization of mice with Mycobacterium bovis strain BCG followed by challenge with tuberculin. The degree of depression of the cytochrome P-450 system correlates with the levels of interferon induced. passive transfer of exogenous gamma interferon also results in depression of the murine cytochrome P-450 system. In the present study the metabolism of diphenylhydantoin, a drug metabolized by the cytochrome P-450 system, was examined in mice in which gamma interferon was induced. The metabolism of diphenylhydantoin was severely inhibited in mice in which interferon was induced, and the level of inhibition correlated with the liter of gamma interferon induced. Passive transfer of gamma interferon also depressed the metabolism of diphenylhydantoin by the murine cytochrome P-450 system.
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PMID:Effects of passive transfer and induction of gamma (type II immune) interferon preparations on the metabolism of diphenylhydantoin by murine cytochrome P-450. 618 Jan 5

The administration of transfer factor obtained from three donors who had recovered from clinical infections with Mycobacterium xenopi to a patient who had a destructive pulmonary infection with this organism, was associated with the reversal of an unfavorable clinical course. Cavitary tuberculosis associated with resistance to all combinations of antituberculosis drugs was probably related to a concurrent depression of cell-mediated immunity of unknown origin. Antigen specific but not nonspecific transfer factor caused a rapid and prolonged improvement in both the pulmonary disease and the immunologic deficiency. Cross-reactivity between the antigenic determinants of M. xenopi and Mycobacterium tuberculosis made it possible to use transfer factor obtained from donors responsive to purified protein derivative of tuberculin. This study clearly demonstrates the additional benefits to be gained from using transfer factor that is antigen-specific in the treatment of infectious diseases.
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PMID:Clinical and immunologic response to antigen-specific transfer factor in drug-resistant infection with Mycobacterium xenopi. 618 88

A previously healthy patient with classic hemophilia who was on a home infusion program with factor VIII concentrates developed an acquired immunodeficiency syndrome manifested by a dramatic weight loss (47 kg over 12 months), lassitude, transient thrombocytopenia, and opportunistic infections with Varicella zoster, Pneumocystis carinii, and Mycobacterium avium-intracellulare. The patient was not homosexual and had no history of intravenous drug abuse. Immunologic studies showed a persistent lymphopenia with reversal of helper/suppressor-cytotoxic T-lymphocyte ratios, depression of human natural killer cell function, and in-vitro lymphocyte proliferative responses to mitogens and viral antigens. Serum IgA levels were also elevated. Serum antibodies against cytomegalovirus, herpes simplex viruses 1 and 2, Epstein-Barr virus, Varicella zoster, and hepatitis B virus were shown, suggesting previous infection by these agents. Reactivation of cytomegalovirus infection was suggested by a rising titer of antibodies against cytomegalovirus concurrent with pneumocystis pneumonia, and was confirmed by the growth of this virus in a throat culture 2 months later.
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PMID:Acquired immunodeficiency syndrome with Pneumocystis carinii pneumonia and Mycobacterium avium-intracellulare infection in a previously healthy patient with classic hemophilia. Clinical, immunologic, and virologic findings. 629 53

Mice injected with 1 mg (about 1 X 10(7) CFU) of Mycobacterium bovis BCG in the footpad showed high levels of delayed-type hypersensitivity (DTH) to BCG antigens and a continuous increase in circulating specific anti-immunoglobulin G (IgG) antibodies throughout a 6-week observation period. In contrast, mice injected intravenously with a 1-mg dose failed to mount a DTH and showed a depression in antibody production at week 5 postinfection. A dose-response study revealed that an optimum dose of BCG, when injected intravenously, can induce a small but significant DTH response. The delayed cutaneous unresponsiveness in intravenously infected mice lasted at least 6 weeks and was not antigenically specific, in that it depressed the DTH response to Corynebacterium parvum. No simple relationship existed between levels of DTH and the amount of circulating anti-IgG antibodies. Splenectomy and treatment with a high dose of cyclophosphamide before infection, although greatly reducing the humoral response, did not reverse the BCG-induced unresponsiveness nor enhance levels of DTH in mice infected in the footpad. It is concluded that the intravenous infection of mice with BCG exerts a nonspecific inhibitory effect on delayed-type immune reactions by the induction of some type of suppressor mechanisms that are resistant to cyclophosphamide.
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PMID:Cutaneous unresponsiveness to Mycobacterium bovis BCG in intravenously infected mice. 634 89

In vivo induction of gamma interferon (IFN-gamma) by sensitization of mice with Mycobacterium bovis strain BCG and subsequent challenge with tuberculin depressed the ability of liver homogenates from treated animals to metabolically activate promutagens. The Ames Salmonella typhimurium revertant assay was used for analyses of metabolic conversion of promutagens by liver homogenates. Relative to the mutant frequencies determined with control liver homogenates, induction of IFN-gamma depressed the abilities of homogenates from treated animals to activate N-acetylaminofluorene (AAF), aflatoxin B1 (AFB1), and benzo[a]pyrene (BP) by 55%, 44% and 95%, respectively. Within 18-24 h of Aroclor 1254 treatment, liver P-450 content had increased 43%, and the relative mutant yields per unit protein for all three promutagens had approximately doubled. In vivo induction of IFN-gamma suppressed the Aroclor 1254-dependent increases in mutagenesis by AAF (63%), AFB1 (90%), and BP (reduced to a level 23% below non-Aroclor 1254 treatment). In all cases, the levels of depression of promutagen activation qualitatively correlated with cytochrome P-450 content and the induction of IFN-gamma.
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PMID:Gamma interferon induction depresses murine hepatic promutagen/procarcinogen activation. 641 4

Adjuvant arthritis was induced in rats by the injection of Mycobacterium tuberculosis, and its severity was scored according to the macroscopic findings of the legs, tails, and ears. The average score so obtained was lower when the rats also received indomethacin (1.5 mg/kg/day). The depression of the albumin/globulin ratio was inhibited significantly by the administration of indomethacin. The levels of acid phosphatase and beta-glucuronidase were elevated after the injection of an adjuvant, but they decreased to some extent in rats administered indomethacin. The levels of thiobarbituric acid (TBA)-reactive substances in the sera and synovia were elevated at 2 weeks after the injection of adjuvant and decreased thereafter. In rats administered 1.5 mg/kg of indomethacin, the increase in both serum and synovial levels of TBA reactants was inhibited significantly. These observations suggest that the aggravation of adjuvant arthritis may be associated with lipid peroxidation and that indomethacin may, in part, exert its anti-inflammatory effect by preventing lipid peroxide-induced damage of the synovial membrane.
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PMID:Lipid peroxidation in rat adjuvant arthritis and its inhibition by indomethacin. 643 68

Lymphocytes from peripheral blood were isolated from leprosy patients and healthy contacts (HC) of leprosy patients and stimulated in vitro with: Mycobacterium leprae and a M. leprae cell wall antigen, MLW 1; tuberculin purified protein derivative (PPD); antigens prepared from Candida albicans, Entamoeba histolytica, Leishmania aethiopica, and parotitis virus; the non-specific mitogens phytohemagglutinin (PHA) and concanavalin A (Con-A). Lymphocytes from patients with untreated lepromatous leprosy failed to respond to the M. leprae antigens, and the median response to PPD was also significantly (p less than 0.005) lower than in the HC group. They responded almost as well as the other groups to non-mycobacterial antigens, PHA, and Con-A. In LL patients who had been treated with dapsone for several (median 10) years, the failure to respond to M. leprae antigens remained, but the depression of the PPD response and the slight non-specific depression of the lymphocyte stimulation test (LST) responsiveness had been reversed. Our results confirm that the major defect in the cell-mediated immune response of LL patients is M. leprae-specific and permanent. The possibility that the defect may be due to a continuous, antigen-induced suppression of the immune response is discussed. That the defect also affected the response to PPD is important since it points to a clear antigenic relationship between M. leprae and BCG/M. tuberculosis. Evidence is presented suggesting that an antigen induced suppressor mechanism may be operating in vitro with cells from patients with borderline tuberculoid leprosy.
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PMID:In vitro lymphocyte stimulation in patients with lepromatous and borderline tuberculoid leprosy. The effect of dapsone treatment on the response to Mycobacterium leprae antigens, tuberculin purified protein derivative and non-mycobacterial stimulants. 676 3

The induction and passive transfer of interferons have been shown to depress the level of cytochrome P-450 drug metabolism system of liver microsomes. Inducers of alpha or beta (Type I) interferons, such as Tilorone-HCl, statalon, mengovirus and others, suppressed the cytochrome P-450 system of rats or mice after administration. Induction of gamma (Type II) interferon also resulted in depression of the cytochrome P-450 system of mice. The gamma interferon was induced by sensitization of mice with Mycobacterium bovis strain BCG followed by challenge with tuberculin. The degree of depression of the cytochrome P-450 system correlated with the levels of interferon induced. In addition, passive transfer of exogenous gamma interferon also resulted in depression of the murine cytochrome-450 system. The metabolism of diphenylhydantoin, a drug metabolized by cytochrome-450, was examined in mice in which gamma interferon was induced. The metabolism of diphenylhydanoin was severely inhibited in mice which interferon was induced, and the level of inhibition correlated with the titer of gamma interferon induced. Passive transfer of gamma interferon also depressed the metabolism of diphenylhydantoin by murine cytochrome P-450.
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PMID:Effects of interferon on drug metabolism. 681 39

D-penicillamine (D-PA) has beneficial therapeutic effects for patients with rheumatoid arthritis but no convincing explanation has been offered for the mode of action. Experiments reported here were designed to gain an insight into the related mechanisms. Wistar rats were inoculated with various doses of Mycobacterium tuberculosis to induce adjuvant arthritis, and on the 21st day, the lesions of paws and ears were graded according to the extent of the erythema and swelling. Rats given D-PA simultaneously with the inoculation of M. tuberculosis developed a more severe arthritis than that seen in the control group, when they were inoculated with low doses of M. tuberculosis. To investigate the effect of D-PA on hemolytic plaque forming cells (PFC) in the spleen, BDF1 mice were immunized with various doses of sheep red blood cells (SRBC) and D-PA was injected in various doses and at various times. D-PA produced either enhancement or depression of the number of PFC, depending on the dose of antigenic stimulus of SRBC. Furthermore, D-PA slightly enhanced the concanavalin A-induced blastogenesis of the spleen cells in vitro, at a concentration of 1-50 microM, but at concentrations of 500 microM, inhibition was evident. These results indicate that D-PA may act as an immunomodulating agent.
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PMID:Studies of D-penicillamine (3): immunomodulating effects of D-penicillamine. 682 Mar 51


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