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)

Mycobacterium tuberculosis and Mycobacterium leprae, the causative agents of tuberculosis and leprosy, respectively, produce large quantities of lipoarabinomannan (LAM), a highly immunogenic, cell wall-associated glycolipid. This molecule has been previously reported to be a potent inhibitor of gamma interferon-mediated activation of murine macrophages. Studies of the mechanism by which this mycobacterial glycolipid down-regulates macrophage effector functions provide evidence that LAM acts at several levels and that it can (i) scavenge potentially cytotoxic oxygen free radicals, (ii) inhibit protein kinase C activity, and (iii) block the transcriptional activation of gamma interferon-inducible genes in human macrophage-like cell lines. These results suggest that LAM can inhibit macrophage activation and triggering and cytocidal activity and that it may represent a chemically defined virulence factor contributing to the persistence of mycobacteria within mononuclear phagocytes.
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PMID:Lipoarabinomannan, a possible virulence factor involved in persistence of Mycobacterium tuberculosis within macrophages. 185 Mar 79

The ability of soluble factors to modulate the growth of a virulent strain of Mycobacterium avium in murine peritoneal macrophages was studied. The virulent strain, TMC 702, grew progressively in the organs of susceptible BALB/C mice. In addition, this strain of M. avium grew progressively in untreated peritoneal macrophages. Treatment of macrophage monolayers with interferon-gamma (IFN-gamma) did not change significantly the intracellular growth of M. avium. Addition of indomethacin to IFN-gamma-treated macrophage monolayers rendered them significantly more bacteriostatic than macrophages treated with interferon alone, suggesting a role for prostaglandins in inducing unresponsiveness to IFN-gamma in infected cells. Additionally, treatment with tumour necrosis factor-alpha led to a modest increase in bacteriostasis, as compared to untreated monolayers. Further experiments with recombinant interleukins showed that interleukin-4 (IL-4), on its own, could increase bacteriostatic activity against M. avium in a reproducible fashion. Experiments with interleukin combinations showed that IFN-gamma and IL-4 treatment of macrophages rendered these cells almost fully bacteriostatic against M. avium, inclusion of scavengers of reactive oxygen species did not modify the beneficial effect of IFN-gamma and IL-4. Overall, our results suggest an important role for interleukins in modulating the interaction between virulent mycobacteria and murine macrophages.
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PMID:Modulation of Mycobacterium avium growth in murine macrophages: reversal of unresponsiveness to interferon-gamma by indomethacin or interleukin-4. 189 13

Acquired resistance to Mycobacterium leprae, the etiologic agent of leprosy, crucially depends on cellular immune mechanisms. In addition to interleukin-mediated helper functions, killer mechanisms seem to be involved. This study addresses the question of how M. leprae render mononuclear phagocytes and Schwann cells, its natural targets, susceptible or resistant to killer cells. Killer activities were stimulated in peripheral blood mononuclear cells from healthy individuals by incubation with mycobacteria plus interleukin-2. These cells lysed Schwann cells and mononuclear phagocytes which had been pulsed with dead M. leprae, while unpulsed targets remained virtually unaffected. Importantly, targets infected with viable M. leprae were not lysed; furthermore, infection with viable M. leprae as well as gamma interferon stimulation or heat shock caused resistance in otherwise susceptible targets which had been pulsed with dead M. leprae. Thus, M. leprae markedly influenced the effect of killer cells on Schwann cells and mononuclear phagocytes.
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PMID:Mycobacterium leprae renders Schwann cells and mononuclear phagocytes susceptible or resistant to killer cells. 189 12

Mycobacterium lepraemurium grew progressively in monolayers of Proteose Peptone-elicited macrophages from C57BL/6 mice. Treatment of macrophage monolayers with gamma interferon led to an enhancement of growth of M. lepraemurium in macrophages. Treatment with tumor necrosis factor alpha or granulocyte-macrophage colony-stimulating factor led to restriction of mycobacterial growth in macrophages.
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PMID:Modulation of Mycobacterium lepraemurium growth in murine macrophages: beneficial effect of tumor necrosis factor alpha and granulocyte-macrophage colony-stimulating factor. 189 14

A 25 kDa glycolipoprotein from Mycobacterium tuberculosis has been shown to inhibit phagocyte functions associated with antimicrobial activity. These include the intracellular killing ability, reduction of nitro blue tetrazolium, hydrogen peroxide production and lysosyme release of polymorphonuclear leukocytes and peripheral blood monocytes. The present study undertook to investigate the synergistic effects of gamma interferon and clofazimine on restoring the inhibitory activities of the 25 kDa glycolipoprotein on these phagocyte functions. Gamma interferon and clofazimine at concentrations of 25 units/ml and 0.3 micrograms/ml acted synergistically by completely restoring all these systems. Independent use of these agents were unable to affect phagocyte functions or to restore the inhibition caused by the 25 kDa mycobacterial component. These studies indicate the possible use of these two phagocyte priming agents for the immunotherapy of tuberculosis.
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PMID:The synergistic effects of gamma interferon and clofazimine on phagocyte function: restoration of inhibition due to a 25 kilodalton fraction from Mycobacterium tuberculosis. 190 25

Murine bone marrow-derived macrophages are able to inhibit the growth of Mycobacterium bovis after stimulation with recombinant gamma interferon. This antimycobacterial activity was inhibited by NG-monomethyl-L-arginine, a specific inhibitor of nitrite and nitrate synthesis from L-arginine. Furthermore, there was a complete lack of mycobacterial growth inhibition in a medium deficient in L-arginine. Nitrite is generated by gamma interferon-activated bone marrow-derived macrophages after infection with M. bovis, and a correlation between mycobacterial growth inhibition and nitrite production was observed. These results indicate that reactive nitrogen intermediates derived from L-arginine are crucially involved in macrophage antimycobacterial activity.
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PMID:Mechanisms involved in mycobacterial growth inhibition by gamma interferon-activated bone marrow macrophages: role of reactive nitrogen intermediates. 190 29

A sandwich ELISA for the detection of gamma interferon showed higher sensitivity and specificity than an indirect ELISA for mycobacterial antibodies in the diagnosis of bovine tuberculosis. Circumstantial evidence of an inverse relationship between cellular and humoral immune responses to Mycobacterium bovis was found in cattle with natural infection.
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PMID:Reciprocal cellular and humoral immune responses in bovine tuberculosis. 190 47

Mycobacterium avium-M. intracellulare is a frequent cause of late disseminated infection in patients with AIDS. The ability of human peripheral blood monocytes to phagocytose and kill M. avium was examined in an in vitro model. Monocytes were obtained from 13 healthy volunteers and 11 patients with AIDS, three of whom had documented disseminated M. avium infection. Monocytes were precultured for 2 days before infection with two AIDS-associated and two non-AIDS-associated strains of M. avium. Uptake of M. avium as measured by counting intracellular acid-fast bacilli did not differ among healthy subjects, patients with AIDS, or patients with AIDS and previously documented disseminated M. avium infection. Intracellular growth of M. avium was examined by a CFU assay of cell lysates from M. avium-infected monocytes after 0, 4, and 7 days of culture. Intracellular growth inhibition of M. avium at 7 days after infection was comparable between patients with AIDS and healthy donors for all M. avium strains tested. The effects of the addition of recombinant gamma interferon on M. avium uptake and intracellular growth in monocytes also were studied. Pretreatment of monocytes with gamma interferon prior to infection suppressed monocyte phagocytosis of M. avium. Continuously coculturing of monocytes with gamma interferon after infection augmented killing of M. avium among both patients with AIDS and healthy controls for three of the four strains of M. avium tested. The magnitude of this effect, however, was variable from donor to donor and strain to strain. No significant differences were noted between the growth-inhibiting abilities of gamma-interferon-treated monocytes obtained from healthy volunteers and those obtained from patients with AIDS.
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PMID:Preservation of monocyte effector functions against Mycobacterium avium-M. intracellulare in patients with AIDS. 191 11

The primary beta-cell antigen of insulin-dependent diabetes is thought to be a protein with a molecular weight of approximately 64 kD. Hyperthermic incubation and cytokines such as interleukin 1 beta, gamma interferon, and tumour necrosis factor induce synthesis of 64 kD protein by insulinoma cells. By western blot techniques, cross-reactivity was found between this 64 kD protein and monoclonal antibodies directed against Mycobacterium tuberculosis heat-shock protein 65, but not with antibodies directed against a similar epitope of M leprae heat-shock protein 65. Binding of M tuberculosis heat-shock protein 65 antibodies to interleukin-1 beta-treated cells was inhibited by prior addition of serum from insulin-dependent diabetic patients which contained antibodies to 64 kD beta-cell antigen. It is suggested that heat-shock protein 65 may be the 64 kD beta-cell antigen and that autoreactivity to an epitope of heat-shock protein 65 may confer susceptibility to insulin-dependent diabetes mellitus.
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PMID:Heat-shock protein 65 as a beta cell antigen of insulin-dependent diabetes. 197 88

Susceptible BALB/c mice were infected with Mycobacterium avium TMC 702. Groups of mice were then infused with 10(4) U (approximately 400 U/h) of murine beta interferon (IFN-beta) via a minipump system, and the progression of the infection was assessed. Mice infused with IFN-beta showed superior resistance to infection, as determined by reduced bacterial growth in the livers and spleens of infected animals, (1-log reduction in bacterial CFU at 2 months postinfection; P less than 0.001). This was corroborated by the fact that resident peritoneal macrophages treated with IFN-beta in vitro (10(2) U/ml) were more bacteriostatic for M. avium TMC 702 than their untreated counterparts. Overall, these findings suggest an important role for IFN-beta in mycobacterial infections.
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PMID:Recombinant murine beta interferon enhances resistance of mice to systemic Mycobacterium avium infection. 201 46


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