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)

Immunosuppressor activity of considerable potency and complexity was generated during the course of chronic, progressive infection of C3H/Anf mice by Mycobacterium lepraemurium. From the 5th through 10th week after inoculation, spleen cells from infected mice mildly but reproducibly suppressed the direct plaque-forming cell response of normal spleen cell cultures to sheep erythrocytes. Suppression at this stage of infection was mediated by cells with macrophage-like characteristics. A marked increase in splenic suppressor activity at 10 to 11 weeks was associated with the appearance of a second suppressor cell subpopulation composed of T lymphocytes. The appearance of these cells was closely related in time to the onset of rapid splenic enlargement and a loss of cutaneous delayed type hypersensitivity to antigens of M. lepraemurium in mice at 10 to 11 weeks of infection. Suppressor cells were not present in peripheral lymph nodes until terminal infection at 22 to 25 weeks. Suppressor spleen cells depressed the T-dependent antibody response most severely, but there was also a direct effect upon B cells as shown by moderate suppression of responses to TNP-LPS and DNP-Ficoll. Spleen cells from 14-week-infected mice generated a soluble suppressor factor(s) that induces depression of moderate severity, however, the immunosuppression by intact cells was far greater.
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PMID:The evolution of immunosuppressive cell populations in experimental mycobacterial infection. 35 Oct 57

1 Subcutaneous injection of Mycobacterium butyricum suspended in mineral oil into the mouse hind paw caused an oedematous local inflammation. Hind paw swelling was maximum 5 days after injection and was still apparent at day 30. 2 Drug metabolism in vivo (as monitored by ketamine- or pentobarbitone-induced sleeping times) was not affected by the inflammatory disease. However, administration of ketamine or pentobarbitone at day 1 led to significantly elevated sleeping times when the mice showing local inflammation were retested at day 5 with the anaesthetics. 3 Indomethacin inhibited hind paw oedema in the mouse but did not affect ketamine-Mycobacterium butyricum-induced depression of drug metabolism. 4 Prolongation of ketamine-induced anaesthesia by combination with Mycobacterium butyricum at day 5 correlated with the degree of hind paw inflammation at this time. 5 The data suggest that anaesthetics (i.e., ketamine and pentobarbitone) may sensitize hepatic membranes to the effect of Mycobacterium butyricum or some toxic compound elaborated during the active phase of inflammation.
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PMID:Depression of drug metabolism in the mouse by a combination of Mycobacterium butyricum and anaesthetics. 76 Aug 85

The influence of dexamethasone and cyclophosphamide on the goat immune system was investigated. Seven goats, with a previous contact with caprine herpesvirus type 1 (CHV-1), were used. All had been vaccinated with live Mycobacterium paratuberculosis vaccine. Six goats were injected intravenously (i.v.) with dexamethasone daily for 5 days (2.5-4 mg/kg BW per day). Three also received 25 mg/kg BW of cyclophosphamide on day 0. The seventh goat was not treated. Dexamethasone alone caused depression, slight lymphopenia and fall in tuberculin reaction. Dexamethasone plus cyclophosphamide caused a severe clinical reaction, marked leukopenia (lymphopenia and polymorphopenia), fall in tuberculin reaction and significant increase in CHV-1 neutralizing antibody titres. M. paratuberculosis antibody reaction was variable and thus difficult to be assessed. CHV-1 was not isolated.
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PMID:Immunosuppression in goats by dexamethasone and cyclophosphamide. 133 Apr 22

Acyl-CoA carboxylase activity in four pathogenic mycobacteria and Mycobacterium smegmatis was shown with both acetyl-CoA and propionyl-CoA substrates. Only very low activity was detected in mycobacteria grown in host tissues or on egg-based media rich in lecithin and avidin. This appeared to be a result of severe depression of activity, as strains which could be grown both in host tissue and egg-based media, and in the relatively simple Dubos or Sauton's media showed 8 to 120-fold higher activity in the simpler media.
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PMID:Control of acyl-CoA carboxylase activity in mycobacteria. 153 46

In eight (25%) of 32 consecutive AIDS patients between 1986 and 1989, Mycobacterium avium infection was diagnosed: in seven disseminated, in one as a local lymph node process. Six patients were treated as consistently as possible with a combination of ethambutol, rifabutine, clofazimine and protionamide (or cycloserine) in relatively large dosages. Median survival of treated patients was 15.5 (4-22) months. Protionamide inhibited most M. avium strains (7 of 8) in vitro, but often caused intolerance (nausea). Treatment of disseminated cytomegalovirus infection in our opinion was necessary in 5 of 6 patients during longterm M. avium therapy. HIV therapy (Zidovudine) during M. avium treatment was not possible due to bone marrow depression. A low maintenance dose of corticosteroids was necessary in 3 of 6 patients (one with adrenal insufficiency) to suppress symptoms such as fever and malaise.
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PMID:[Mycobacterium avium disease in AIDS patients; diagnosis and therapy]. 175 16

NIH mice infected with Mycobacterium lepraemurium (MLM) show a marked depression in their levels of hemolytic complement that is proportional to the degree of infection. The defect affects more the activation of complement through the classical pathway (CPW) than the activation of complement through the alternative pathway. Although this low activity of CPW-complement may be due to different causes (complement consumption by the infecting microorganism, lack of biosynthesis of complement components, or the presence of complement inhibitory factors), our results seem to support the last possibility. The generation of factors in the infected animals that inhibit the autologous activity of complement as the infection goes on reduces the risk of complement-mediated tissue damage and prolongs the survival time of the host, a wise strategy on the part of the MLM to assure its own survival as a parasite.
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PMID:Inhibition of complement activity in murine leprosy. 180 43

Spleen cells of Mycobacterium lepraemurium-infected mice were cultured on petri dishes coated with mycobacterial antigens, and antigen-reactive cells were isolated. Upon incubation in mitogen- or antigen-free culture medium, these cells released mediators capable of depressing the in vitro proliferative response of normal splenocytes to specific antigen and to concanavalin A and lipopolysaccharide. One of these mediators was identified with gamma interferon (IFN-gamma), mainly on the basis that treatment of supernatants with monoclonal anti-IFN-gamma antibodies markedly reduced the suppressive activity contained therein. Detectable levels of tumor necrosis factor alpha (TNF-alpha) and TNF-beta were present in spleen cell culture supernatants of infected mice. Moreover, low doses of recombinant TNF-alpha and TNF-beta were found to potentiate the suppressive activity of exogenous IFN-gamma. Soluble T-cell receptors beta were also detected in the culture supernatants. The elimination of these molecules with monoclonal anti-T-cell receptor beta (F23.1) antibodies immobilized on a plastic surface partially reversed the depression of the response to mycobacterial antigen but did not affect the response to mitogens. These results revealed the complex nature of suppressor mediators that are produced by mycobacterial antigen-reactive cells and that regulate the in vitro proliferative response.
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PMID:A role for gamma interferon, tumor necrosis factors, and soluble T-cell receptors in the depressed blastogenic response of spleen cells of Mycobacterium lepraemurium-infected mice. 183 61

The phenotype of inflammatory cells in lymph nodes from 16 patients with culture-proven tuberculous lymphadenitis were examined by histological and immunohistochemical techniques. Eight patients were suffering from a symptomatic HIV1 infection and 8 patients were immunocompetent individuals without positive HIV1 serology. In addition, the lymph nodes of 2 AIDS patients with Mycobacterium avium-intracellulare infection were examined using the same techniques. Characteristic granulomas with or without caseation were observed in the 8 immunocompetent and the 4 HIV1-infected patients with less marked lymphopenia of CD4+ peripheral blood lymphocytes (PBL). In lymph nodes from the other HIV1-infected patients with more severe depression of CD4+ PBL, no epithelioid cell formation was present; instead, foamy macrophages were found. The phenotype of the macrophages underwent progressive changes in parallel with the decreasing numbers of CD4+ PBL. Foamy macrophages in M. avium-intracellulare infection exhibited remarkable erythrophagocytotic activity and may represent an end-stage phenotype. They were positive for S100 protein and did not produce lysozyme or alpha-1-antichymotrypsin. They lost the antigen which was detected by monoclonal antibody Mac387 whereas positivity for HLA-DR, CD68 and KI-M8 was preserved. While many lymphocytes expressed CD25 (IL2 receptor) in cases with typical granulomas, there was no such CD25 expression in cases without epithelioid cell formation. Although granulomas have been produced in experimental animals independently of cell-mediated immune mechanisms, our results suggest that T-cell functions are necessary for epithelioid granuloma formation in human tuberculosis.
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PMID:In situ immunophenotype of macrophages and lymphocytes in granuloma formation of tuberculous lymphadenitis in HIV-infected and immunocompetent patients. 189 41

For many years tuberculosis has been known to occur with greater frequency among persons with disorders that impair host defenses. In most instances these processes interfere with the immune response to Mycobacterium tuberculosis, whereas, in a few, such as silicosis, the probable abnormality is a nonimmune defect in macrophage function. Infection with the human immunodeficiency virus (HIV) causes progressive and ultimately profound depression of both humoral and cell-mediated immunity and, thus, is an extremely potent risk-factor for tuberculosis. Presumably the major effect of HIV infection that predisposes persons to developing tuberculosis is the reduction in circulating T-helper (CD4+) lymphocytes which causes a reduction in cytokine production and a consequent decrease in the functional capabilities of macrophages. However, a number of questions concerning pathogenesis of tuberculosis related to HIV remain. Available data suggest that the magnitude of the risk for developing tuberculosis among persons infected with both HIV and M. tuberculosis is very high, 8% in one prospective study. Because of the epidemic of HIV infection, the progressive downward trend in the incidence of tuberculosis in the United States has reversed and in 1989 there was a 5% increase in the number of cases. Preliminary data for 1990 suggest that there will be an 8 to 10% increase over 1989. Also in the United States approximately 3% of tuberculosis patients have been found to be HIV seropositive. The clinical features of tuberculosis in patients with HIV infection vary depending on the degree of immunosuppression. With mild immunosuppression early in the course of HIV infection tuberculosis presents in a "typical" way with positive tuberculin skin tests, upper lobe cavitary infiltrates on chest film and positive sputum smears and cultures. As the HIV infection progresses, the mode of presentation of tuberculosis becomes more "atypical" with negative skin tests, multiple sites of involvement, chest films showing diffuse noncavitary infiltrates often accompanied by intrathoracic lymphadenopathy. The key to diagnosis is maintaining a high index of suspicion for tuberculosis, especially in patients with advanced HIV disease and including appropriate laboratory examinations in the evaluations of such persons. Regardless of the stage of HIV infection the response to treatment for tuberculosis is generally favorable if it is begun promptly. Standard therapy utilizing isoniazid, rifampin, and pyrazinamide with or without ethambutol have been associated with high rates of cure. Relapse has been uncommon. There has been, however, at least one outbreak of tuberculosis caused by isoniazid and rifampin resistant organisms in which the response to therapy was very poor.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical features, diagnoses, and management of tuberculosis in immunocompromised hosts. 194 27

Immunosuppressive mechanisms loom as important factors in depression of delayed-type hypersensitivity responses during active tuberculosis. Nonspecific suppression may be mediated by circulating immune complexes containing mycobacterial polysaccharides such as D-arabino-D-galactan. The mechanism of suppression involves activation of monocyte production of immunosuppressive prostaglandin E2. Peripheral blood mononuclear cells from patients with tuberculosis include increased numbers of monocytes that suppress the response to tuberculin purified protein derivative (PPD). Antigen-specific suppression is associated with monocyte activation by a number of criteria, including decreased surface expression of HLA-DR determinants and increased production of interleukin 1 (IL-1). The increased production of IL-1 is associated with--and may have a causal relation to--immunosuppression. A second parallel regulatory mechanism involves PPD-specific suppression by Fc gamma receptor-bearing lymphocytes. The consequence of these immunosuppressive circuits is depression of tuberculin-induced blastogenesis, production of IL-2, and generation of IL-2 receptors. These findings suggest that natural infection with Mycobacterium tuberculosis may result in immunosuppression. Studies of potentially protective antigens in experimental systems must be designed to assess and avoid activation of suppressor circuits.
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PMID:Immunologic aspects of mycobacterial infections. 246 22


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