Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026918 (Mycobacterium)
 52,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A protein preparation, from culture filtrates from a strain of Mycobacterium kansasii (MK precipitate), which cross reacts with antibodies to human chorionic gonadotropin (hCG) beta subunit and antibodies to cholera toxin beta subunit, has been isolated. A tissue culture assay was used to detect the ability of this preparation to affect the antiviral activity of interferons and to visualize changes in cell shape and cell-cell contact caused by this preparation. A cholera toxin containing precipitate (CT precipitate) from cultures of Vibrio cholerae and commercially prepared hCG were used for comparison. It was found that MK, CT, and hCG may cause reduction or apparent enhancement of interferon antiviral activity or may have no effect. The effect that is observed depends on which test protein the cells are treated with, the type of interferon used, and which cell line is employed in the assay. All three protein preparations had visible effects on the shapes of the cells and the way the cells interacted to form a monolayer.
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PMID:A protein preparation from Mycobacterium kansasii culture filtrate has biological activity similar to that of hCG and cholera toxin in human cell lines. 244 70

Bone marrow-derived murine macrophages are able to inhibit the growth of Mycobacterium bovis and of some strains of M. tuberculosis after stimulation with either recombinant gamma interferon (rIFN-gamma) or lymphokines from antigen-specific T-cell clones. To elucidate the mechanism(s) involved in antimycobacterial activity, macrophages were infected with M. bovis in the presence of agents thought to influence the antimicrobial effects of phagocytes. Scavengers of toxic oxygen metabolites failed to influence the capacity of IFN-gamma-activated bone marrow macrophages to inhibit the growth of M. bovis. Suramin slightly affected mycobacterial growth in IFN-gamma-activated macrophages, and chloroquine markedly induced growth inhibition of M. bovis in unstimulated macrophages. We conclude that growth inhibition of M. bovis by IFN-gamma-activated macrophages is an oxygen-independent process.
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PMID:Attempts to characterize the mechanisms involved in mycobacterial growth inhibition by gamma-interferon-activated bone marrow macrophages. 245 66

Mice inoculated intravenously with trehalose-6,6'-dimycolate (TDM), a glycolipid component of the cell wall of Mycobacterium, in an oil-in-water emulsion (TDM emulsion) acquired a high resistance to intranasal infection by influenza virus. Athymic nude mice inoculated with TDM emulsion could not acquire such an augmented resistance to influenza virus infection. The augmented antiviral resistance of TDM emulsion-treated mice was diminished by prior intravenous inoculation of silica particles, which selectively impair macrophage functions. In vitro experiments showed that macrophage cultures treated with TDM emulsion released an activator(s) of T lymphocytes. Histological studies of the lung of TDM emulsion-inoculated mice revealed that a typical granuloma and severe perivascular lymphocyte infiltration appeared, though no such histological change was observed in the lung of control emulsion-inoculated mice. The lungs from TDM emulsion-treated athymic nude mice and the lungs from silica particle- and TDM emulsion-treated mice showed fewer and smaller granulomata and milder perivascular lymphocyte infiltration than a typical granuloma and lymphocyte infiltration in the lungs of TDM emulsion-treated mice. These and earlier results suggest that an acquired antiviral resistance of TDM emulsion-treated mice was caused by elicitation of macrophages with TDM, then activation of T lymphocytes, leading to granuloma formation and an amplified earlier interferon production in response to influenza virus infection.
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PMID:Correlation between augmented resistance to influenza virus infection and histological changes in lung of mice treated with trehalose-6,6'-dimycolate. 246 May 92

We have found that natural killer (NK) cells were very active in pleural effusions containing Mycobacterium tuberculosis. Cytotoxicity against K562 and Raji was augmented when the mononuclear cells were cocultured for 18 hr with purified protein derivative (PPD) derived from M. tuberculosis culture supernatants. In pleural effusions of cancer patients, PPD-activated mononuclear cells were less cytotoxic than their counterparts in peripheral blood. However, in the same patients, interferon and interleukin-2 production was greater in pleural effusions than in peripheral blood. On the other hand, in tuberculosis patients there was no significant difference in cytotoxicity between peripheral blood and pleural effusion mononuclear cells, but the production of interferon and interleukin-2 was higher in pleural effusions than in peripheral blood. Neither group of patients consistently demonstrated a correlation between production of interferon or interleukin-2 in peripheral blood and cytotoxicity. Both PPD-induced cytotoxicity and the production of interferon and interleukin-2 were lower in mononuclear cells of carcinomatous than tuberculous pleural effusion. These results indicate that peripheral blood and pleural effusion mononuclear cells differ in cytotoxicity as well as in interferon and interleukin-2 production. Further, these activities also differ in tuberculous and carcinomatous pleural effusions.
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PMID:Purified protein derivative induced cytotoxicity in carcinomatous and tuberculous pleurisy. 246 59

Leprosy is a spectral disease in which clinical presentation is thought to be related to the host immune response. Previous investigations have suggested that selective unresponsiveness to Mycobacterium leprae in patients with lepromatous leprosy is due to the presence of M. leprae-specific T-suppressor cells. However, it has recently been suggested that CD2 modulation was the mechanism for the observed impaired immune response in lepromatous patients. Therefore, we studied the expression of CD2 and CD3 on lymphocytes in lepromatous skin lesions and peripheral blood mononuclear cells (PBMC). Using immunohistochemical techniques, we found that virtually all of the CD3+ cells in leprosy skin lesions expressed CD2. In addition, indirect immunofluorescence flow cytometry demonstrated that most CD3+ cells in the peripheral blood possessed the CD2 marker, suggesting that CD2 expression of T-lymphocytes is normal. T-cell activation using paired anti-T11(2) and anti-T11(3) or anti-CD3 monoclonal antibodies demonstrated similar 3H-thymidine incorporation and gamma interferon production in the PBMC of lepromatous patients in comparison with the PBMC of their contacts and tuberculoid patients. However, lepromatous PBMC did not proliferate or produce gamma interferon in response to M. leprae. Our data suggest not only that CD2 expression is normal on T lymphocytes in lepromatous leprosy skin lesions but also that CD2 expression in peripheral blood lymphocytes is functional in T-cell activation. Defective CD2 modulation does not appear to be the mechanism for specific unresponsiveness in lepromatous leprosy.
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PMID:CD2 expression and function in lepromatous leprosy. 247 3

Mycobacterium avium is a frequent opportunistic pathogen in the acquired immunodeficiency syndrome (AIDS). We compared 12 strains of M. avium in an in vitro model of pathogenicity. Peripheral blood-derived monocytes from healthy individuals were infected with M. avium in vitro. Bacterial uptake and intracellular replication were assessed by microscopic count of acid-fast bacilli and CFU of bacteria, respectively, in lysed monocytes. The CFU assay showed that among five AIDS-associated strains, only one replicated in monocytes. Two of seven non-AIDS-associated strains replicated intracellularly. In addition, we examined the effect of gamma interferon (IFN-gamma) on M. avium infection. IFN-gamma treatment of monocytes decreased phagocytosis and had no effect on the intracellular replication of M. avium. Thus, most strains of M. avium do not multiply within monocytes from healthy individuals and IFN-gamma does not have macrophage-activating factor activity for M. avium infection of human monocytes.
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PMID:Pathogenicity of Mycobacterium avium for human monocytes: absence of macrophage-activating factor activity of gamma interferon. 249 38

Serum from Mycobacterium bovis BCG-infected mice that had been challenged with lipopolysaccharide (LPS) exhibited a marked ability to induce gamma interferon (IFN-gamma) in cultures of spleen cells of normal mice in the presence of interleukin-2 (IL-2). The inducing activity became detectable in the circulatory system about 90 min after LPS challenge, disappeared at around 5 h, and was observable upon 640x dilution of the serum. Addition of monoclonal anti-IL-2 receptor antibody to the culture inhibited the induction by the serum. The activity induced high levels of IFN-gamma even in nylon wool-nonadherent cells, while concanavalin A failed to do so. Serum from uninfected mice challenged with LPS contained no such activity. The molecular weight of the active substance, estimated by gel filtration, was about 70,000. There were pronounced differences among mouse strains in the activities of the sera prepared, which paralleled the amounts of IFN-gamma produced in vivo. However, the levels of IFN-gamma produced in whole spleen cells and in nylon wool-nonadherent cells from mice of various strains were the same when stimulated with competent serum. These results indicate the existence of an unidentified factor that induces IFN-gamma in cooperation with IL-2 in macrophage-depleted splenocytes. They also suggest that IFN-gamma production in vivo is not genetically controlled at the lymphocyte level but, rather, at the level of synthesis of the unknown factor.
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PMID:Endotoxin-induced serum factor that stimulates gamma interferon production. 249 65

This study examined the effects of a 25-kilodalton (kDa) glycolipoprotein derived from Mycobacterium tuberculosis on phagocyte functions associated with antimicrobial activity. The 25-kDa fraction inhibited the ability of both polymorphonuclear cells and cultured monocytes to release lysozyme and produce hydrogen peroxide. In addition, the glycolipoprotein was capable of reducing hexose monophosphate shunt activity and interfered with the ability of polymorphonuclear cells to reduce Nitro Blue Tetrazolium. Inhibition of these antimicrobial systems was optimal at a 50-micrograms/ml concentration of the 25-kDa fraction. Gamma interferon, but not alpha interferon, partially reversed the inhibitory effect of the mycobacterial component in all of the systems assessed. These studies indicate important mechanisms in the understanding of the pathogenesis of tuberculosis and suggest that gamma interferon may have a therapeutic role in mycobacterial diseases.
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PMID:A 25-kilodalton fraction from Mycobacterium tuberculosis that inhibits hexose monophosphate shunt activity, lysozyme release, and H2O2 production: reversal by gamma interferon. 249 74

The killing of Mycobacterium leprae by resting and gamma interferon (IFN-gamma)-activated macrophages in normal subjects and leprosy patients was assessed. Resting macrophages from normal individuals demonstrated the ability to kill M. leprae. For macrophages from tuberculoid patients, killing of M. leprae was only achieved in the presence of IFN-gamma, suggesting that initial T-cell activation occurs prior to the killing of M. leprae. In contrast, though activation with IFN-gamma rendered the lepromatous macrophages microbicidal, it failed to induce lymphocyte proliferation, suggesting a defect at either the antigen-presenting cell or the lymphocyte level or both. The concept that T-cell anergy is primarily due to lack of lymphokine generation was ruled out by our results, since responsiveness was restored in only a small proportion of lepromatous patients after exogenous lymphokine addition. In conclusion, this study demonstrated that killing and antigen presentation are two independent events. It appears that the ability of the macrophages per se to kill M. leprae may be of greater importance than lymphocyte-mediated activation for protection against M. leprae infection.
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PMID:Correlation between macrophage activation and bactericidal function and Mycobacterium leprae antigen presentation in macrophages of leprosy patients and normal individuals. 249 15

Gamma interferon, an immune lymphokine that protects mouse macrophages against infection by several parasites, was ineffective against Mycobacterium lepraemurium. On the contrary, it significantly stimulated multiplication of M. lepraemurium in the macrophages. Simultaneous treatment of macrophages with gamma interferon and interleukin-4 or interleukin-2 or a combination of all three did not enhance the macrophage resistance to infection with M. lepraemurium, but instead stimulated growth of M. lepraemurium.
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PMID:Enhancement of growth of Mycobacterium lepraemurium in macrophages by gamma interferon. 250 Dec 20


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