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)

The depression of the granulomatous response to Mycobacterium bovis strain BCG in mice infected intravenously with 2 x 10(7) CFU of the microorganism turned out to be mediated by various types of cells arising at different times after infection. Anti-PPD B lymphocytes were found to play a major role at Day 1 after infection and to be no longer effective 4 days later. At this time the depression was mediated by anti-idiotype B lymphocytes, whereas T lymphocytes proved to be involved in later phases of the infectious process. These results show that B lymphocytes may be of critical importance in the regulation of cell-mediated immune reactions to this facultative intracellular parasite.
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PMID:B-cell-mediated depression of the granulomatous response to BCG in mice. 264 54

The results shown here demonstrate that in mice heavily infected with Mycobacterium bovis BCG Pasteur, mitogen-induced levels of interleukin-2 (IL-2) correlate temporally with the state of immunity that is being expressed in the animal during the course of the infection. Active immunity, which is conferred by populations of both CD4+ (L3T4) and CD8+ (Lyt-2) T lymphocytes, and memory immunity, which is mediated by a population of CD4+ T lymphocytes, were identified and distinguished in terms of their sensitivity to cyclophosphamide therapy, their ability to passively transfer specific resistance to infection with virulent Mycobacterium tuberculosis, and their capacity to produce and/or absorb IL-2. In this regard, concanavalin A (Con A)-stimulated L3T4+ and Lyt-2+-enriched splenocytes exhibited an apparent depression in measurable levels of IL-2 when harvested during the first 40 days of the infection, which could be explained by the subsequent observation that these T cells were capable of rapidly absorbing a known quantity of recombinant IL-2 in vitro. Detectable levels of IL-2 in these mitogen-stimulated supernatants began to rise after Day 25, which was temporally associated with a gradual shift from active immunity, to immunity mediated by cyclophosphamide-resistant memory T cells, which did not absorb IL-2 in vitro. These data indicate that fluctuations in apparent IL-2 production reflect changes in the type of immunity being expressed, rather than than some form of defect in IL-2 production.
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PMID:Patterns of IL-2 production and utilization in mice heavily infected with Mycobacterium bovis BCG reflect the phase of protective immunity being expressed. 266 9

In acquired immunodeficiency syndrome (AIDS) the pulmonary opportunistic infections are due to the depression of cellular immunity and they are found in more than 50% of patients. Most frequently the infection is due to Pneumocystis carinii, Cytomegalovirus, Cryptococcus neoformans and Mycobacterium avium-intracellulare. Non-opportunistic infections in AIDS are mostly due to the Mycobacterium tuberculosis and Legionella pneumophila. In Kaposi sarcoma in AIDS the lungs may be involved into pulmonary manifestations of the syndrome. In this paper the diagnostics of pulmonary disturbances in AIDS is briefly evaluated together with the therapy of most frequent pulmonary infections.
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PMID:[Pulmonary manifestations in patients with AIDS]. 279 62

The depression of cellular immunity in lepromatous patients is not understood. While the blood monocytes of leprosy patients appear to be activated normally by lymphokines, T cell proliferation and production of lymphokines in response to Mycobacterium leprae are impaired in lepromatous patients. Attempts to restore responsiveness in cells from these patients have been unsuccessful in our hands. The addition of exogenous IL-2 to leukocyte cultures does not appear to restore responsiveness to M. leprae in cells from nonresponder patients. Rather, some enhancement, often not antigen specific, is observed in cells from patients with a preexisting response. Similarly, depletion of monocytes does not restore responsiveness to M. leprae in non-responder patients, but a nonspecific enhancement of proliferation is observed in monocyte-free cultures from patients that do respond to M. leprae. Thus, the defect in lepromatous non-responder patients does not result from a simple lack of IL-2 production or suppression by monocytes and/or their products. Possibly, there is a low level or lack of M. leprae responsive T cells in the circulation of these patients.
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PMID:Cellular immunity in lepromatous and tuberculoid leprosy. 293 94

Mice were infected intravenously with 1.0 mg of Mycobacterium bovis BCG. At various times thereafter, spleen and peripheral lymph node cells were stimulated with concanavalin A for 18 to 20 h, and their capacity to produce interleukin-2 (IL-2) was evaluated by means of a T-cell blast proliferation technique. A depression of IL-2 production that was complete in the spleen but partial in lymph node cell cultures occurred at 2 to 3 weeks and persisted till weeks 8 to 10 after infection. No direct evidence was found for an active suppressor mechanism depressing in vitro the production of IL-2. In spleen cell cultures the suppression of IL-2 production would result from a functional defect of the IL-2-producing T-cell subset, whereas in lymph node cell cultures the depression mainly results from a relative lack of IL-2-producing cells caused by an accumulation of immunoglobulin-positive and "null" cells. Spleen cells from BCG-infected mice maintained their capacity to acquire IL-2 receptors when activated by concanavalin A.
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PMID:Mechanisms underlying the depressed production of interleukin-2 in spleen and lymph node cell cultures of mice infected with Mycobacterium bovis BCG. 308 45

We have investigated the mechanism of the inhibition of phagosome-lysosome (P-L) fusion in macrophages known to occur after infection by Mycobacterium tuberculosis and by the mouse pathogen Mycobacterium microti. We have used an M. microti infection and have studied, first, the saltatory movements of periphagosomal secondary lysosomes by means of visual phase-contrast microscopy (a similar use of the method having been previously supported by computer analyses). The movements became slow or static after ingestion of live but not of heat-killed M. microti. They were unaffected by a fusiogenic mycobacterium M. lepraemurium. Second, we studied the behavior of a normally fusiogenic unrelated organism, Saccharomyces cerevisiae, after its phagocytosis by cells already containing live M. microti ingested 18 h previously. We observed, using a fluorescent assay of fusion, that many of these yeast phagosomes now also failed to fuse with the lysosomes; in contrast, when the host M. microti had been heat killed the yeast phagosomes fused normally. These observations were extended by ultrastructural quantitative analyses of P-L fusion, which confirmed the nonfusion of phagosomes of live M. microti and, more particularly, the change to nonfusion from the normal fusion behavior of the separate phagosomes of accompanying yeasts. Third, we have assembled evidence against the likelihood that these M. microti-induced phenomena are nonspecific, i.e., secondary to a general depression of activity of heavily infected host cells. The evidence includes the feasibility of adjusting the degree of infection so as to facilitate visual assessment of organelle movements without the presence of detectable damage to the cells studied; the absence of lysosomal stasis after comparable infection with another mycobacterium of comparable virulence (M. lepraemurium); and the reversibility of the stasis. We conclude that inhibition of lysosome saltatory movements (and consequently its secondary effect on the associated yeasts) is a significant, specifically induced phenomenon. From these observations and considerations, therefore, in conjunction with the analogous inhibition of lysosomal movements in normal macrophages by some chemical inhibitors of P-L fusion, and our suggestion that this association is causally related, we now suggest that M. microti-induced focal lysosomal stasis is also the main means by which the inhibition of P-L fusion is brought about by this organism. This concept is strengthened by the observations on S. cerevisiae, which provide strong evidence that stasis can cause suppression of fusion.
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PMID:Inhibition of phagosome-lysosome fusion in macrophages by certain mycobacteria can be explained by inhibition of lysosomal movements observed after phagocytosis. 330 28

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, tail, and ears. The average score so obtained was lower in SOD-injected rats than in the control group. The depression of albumin/globulin ratio was inhibited significantly in rats treated with 10.0 mg/kg of SOD. The levels of acid phosphatase and beta-glucuronidase were elevated after the administration of an adjuvant, and these lysosomal enzymes showed a remarkable increase in the control rats, while the elevation was inhibited in rats injected with 10.0 mg/kg of SOD. The levels of TBA-reactive substances in the sera and synovia were elevated at 2 weeks after the injection of adjuvant and decreased thereafter. In rats injected with 5.0 mg/kg or 10.0 mg/kg of SOD, 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 due to superoxide, and that SOD may be beneficial for the treatment of arthritis.
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PMID:The increase of lipid peroxidation in rat adjuvant arthritis and its inhibition by superoxide dismutase. 401 32

Rats given a single subdermal injection into the left hind paw of 0.5 mg Mycobacterium tuberculosis suspended in 0.1 ml of mineral oil, after several days of latency, developed arthritis accompanied by depression in liver microsomal phosphatidylcholine and phosphatidylethanolamine synthesis at 7, 14 and 21 days. The depression of liver microsomal phosphatidylcholine and phosphatidylethanolamine concentrations of experimental animals was accompanied by decreased incorporation of radioactive palmitate into both phospholipids. Nevertheless, the biosynthesis of phosphatidylcholine via the methylation pathway was unaffected. These observations suggest that adjuvant arthritis affects quantitatively the phospholipid composition of the liver endoplasmic reticulum, which consequently may lead to impairment of the microsomal drug-metabolizing enzyme system.
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PMID:The effect of adjuvant-induced arthritis on rat liver microsomal phospholipid metabolism. 407 96

The effects of carbon dust inhalation on the bone marrow-derived (B) and thymus-derived (T) lymphocyte populations of spleen and mediastinal lymph node (MLN) cultures were examined. The concanavalin A (Con A)-responsive cell population (T cells) in the spleen was found to be depressed after 7 days of pre-exposure to carbon dust. However, this effect was transient, and after 14, 21, and 28 days of pre-exposure to carbon dust, the Con A-responsive cells exhibited a 30 to 40% enhancement over control group responses. Conversely, Con A-responsive cells in the pooled MLN cultures exhibited depression, ranging from 22 to 33% below control group values, after 7, 14, and 28 days of pre-exposure to carbon dust. The lipopolysaccharide (LPS)-responsive cell population (B cells) in the spleens of carbon-exposed mice was found not to differ significantly from control group values after all times of pre-exposure. LPS-responsive cells in the MLN cultures exhibited enhancement, ranging from 49 to 74% above control values, after 14, 21, and 28 days of pre-exposure to carbon dust. The ability of carbon spleen cell cultures from carbon-exposed mice to undergo antigen induced blast transformation after sensitization with Mycobacterium tuberculosis H37Ra was also determined. Mice exposed to carbon dust inhalation 2 weeks before and 3 weeks after aerosol or subcutaneous immunization exhibited significantly enhanced ratios of transformation upon culture of their spleen lymphocytes with purified protein derivative of tuberculin.
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PMID:Effects of carbon dust inhalation on the cell-mediated immune response in mice. 420 26

Induction of type II interferon by sensitization of mice with Mycobacterium tuberculosis strain BCG and challenge with tuberculin resulted in a depression of the cytochrome P-450 drug metabolism system of the liver. The degree of depression was significantly greater than in mice that were only sensitized to BCG. Cytochrome b5 levels were not affected. In addition, the level of the depression of the cytochrome P-450 system correlated with the levels of type II interferon induced. Passive transfer of exogenous type II interferon preparations also significantly depressed the cytochrome P-450 system. Passive transfer of mock interferon or of normal serum had no effect.
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PMID:Type II interferon induction and passive transfer depress the murine cytochrome P-450 drug metabolism system. 615 62


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