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Query: UMLS:C0026918 (Mycobacterium)
 52,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six strains of Mycobacterium tuberculosis of different virulence in guinea-pigs were compared with regard to their resistance to low pH, to hydrogen peroxide (H2O2) at different pH values and to superoxide (O2-). Low virulence was associated with susceptibility to H2O2 in native and isoniazid-resistant strains but not in laboratory-attenuated strain H37Ra. H2O2 resistance was only partly related to catalase content. Low virulence was not associated with susceptibility to an acid environment but the tuberculocidal effect of H2O2 was significantly increased at low pH. The strains were uniformly resistant to O2- and contained similar amounts of superoxide dismutase. The implications of these observations are discussed in the context of mechanisms of host defence in tuberculosis.
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PMID:Virulence and resistance to superoxide, low pH and hydrogen peroxide among strains of Mycobacterium tuberculosis. 2 84

Among 58 isoniazid-sensitive strains of Mycobacterium tuberculosis from India, Burma and East Africa, 23 were of phage type A, 31 of type I (intermediate), 4 of type B and none of type C. Type I strains differed from type A strains in being attenuated in the guinea-pig, susceptible to H2O2, sensitive to thiophen-2-carboxylic acid hydrazide and resistant to thiacetazone and p-aminosalicylic acid; the content of strongly acidic lipids and of sulphatide lipids was low and the attenuation indicator lipid was present. The pattern of results with the type B strains did not correspond to the patterns for types A or I. Strains of type I appear to be a distinct group within the species M. tuberculosis.
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PMID:The correlation of bacteriophage types of Mycobacterium tuberculosis with guinea-pig virulence and in vitro-indicators of virulence. 8 Apr 40

Mycobacterium carotenum is more tolerant to the action of hydrogen peroxide than its white, carotenoidless mutant. This elevated tolerance to H2O2 correlates with a higher content of DNA, RNA, and polysaccharides in the cells; it is not related to the content of proteins and lipids, or to the level of the catalase and peroxidase activity.
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PMID:[Tolerance to H202 of Mycobacterium carotenum and its carotinoidless mutant]. 122 42

Tuberculosis remains one of the major infectious causes of morbidity and mortality in the world, yet the mechanisms by which macrophages defend against Mycobacterium tuberculosis have remained obscure. Results from this study show that murine macrophages, activated by interferon gamma, and lipopolysaccharide or tumor necrosis factor alpha, both growth inhibit and kill M. tuberculosis. This antimycobacterial effect, demonstrable both in murine macrophage cell lines and in peritoneal macrophages of BALB/c mice, is independent of the macrophage capacity to generate reactive oxygen intermediates (ROI). Both the ROI-deficient murine macrophage cell line D9, and its ROI-generating, parental line J774.16, expressed comparable antimycobacterial activity upon activation. In addition, the oxygen radical scavengers superoxide dismutase (SOD), catalase, mannitol, and diazabicyclooctane had no effect on the antimycobacterial activity of macrophages. These findings, together with the results showing the relative resistance of M. tuberculosis to enzymatically generated H2O2, suggest that ROI are unlikely to be significantly involved in killing M. tuberculosis. In contrast, the antimycobacterial activity of these macrophages strongly correlates with the induction of the L-arginine-dependent generation of reactive nitrogen intermediates (RNI). The effector molecule(s) that could participate in mediating this antimycobacterial function are toxic RNI, including NO, NO2, and HNO2, as demonstrated by the mycobacteriocidal effect of acidified NO2. The oxygen radical scavenger SOD adventitiously perturbs RNI production, and cannot be used to discriminate between cytocidal mechanisms involving ROI and RNI. Overall, our results provide support for the view that the L-arginine-dependent production of RNI is the principal effector mechanism in activated murine macrophages responsible for killing and growth inhibiting virulent M. tuberculosis.
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PMID:Killing of virulent Mycobacterium tuberculosis by reactive nitrogen intermediates produced by activated murine macrophages. 155 82

BALB/c mice were infected with 10(5) colony forming units (cfu) of Mycobacterium avium TMC 702 i.v. and the growth of the inoculum followed in the spleens of control mice. Other infected mice given weekly doses of 1 microgram of TGF-b1 or weekly doses of 2 mg of a rabbit antiserum against mouse TGF-b1 were evaluated for their resistance to M. avium TMC 702. Growth of M. avium in the spleens of mice given repeated doses of TGF-b1 (1 microgram weekly) was significantly higher than in the spleens of control mice starting at day 40 of infection. Similarly, growth of M. avium was significantly diminished (0.7 log difference at 80 days) in mice given infusions of anti-TGF-b1 (2 mg weekly). Macrophage activation status was similar in the three groups of mice, as seen by a comparable release of superoxide anion (O2-) and hydrogen peroxide (H2O2) by peritoneal macrophages of infected mice. However, TGF-b1-pulsed peritoneal macrophages were found to be more permissive for M. avium growth in vitro than control macrophage monolayers. Overall, these results suggest that TGF-b1 plays a detrimental role in the progression of experimental M. avium infections, by an unclear mechanism.
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PMID:Transforming growth factor beta (TGF-b1) plays a detrimental role in the progression of experimental Mycobacterium avium infection; in vivo and in vitro evidence. 181 90

Following the intraperitoneal inoculation of 2.5 x 10(8) colony-forming units of Mycobacterium avium strain ATCC 25291, there was bacillary growth in the liver, spleen and peritoneal cavity of C57BL/6, C57BL/10, DBA/1 and BALB/c mice whereas DBA/2, C3H/He, CBA/Ca and CD-1 mice controlled the infection showing constant or slightly decreasing numbers of viable bacteria in the liver and spleen and effective clearance of the bacilli from the peritoneal cavities. The acquisition of non-specific resistance (NSR) to Listeria monocytogenes during the infection by M. avium was high in C57BL/6, BALB/c and C3H/He mice and negligible in DBA/2 and CD-1 mice. The magnitude of the acquisition of NSR was reduced in T cell-deficient mice and was directly proportional to the dose of the inoculum of M. avium. The production of hydrogen peroxide by phorbol myristate acetate-stimulated peritoneal macrophages of M. avium-infected mice was higher in C57BL/6 and BALB/c mice than in CD-1, DBA/2 and C3H/He animals. BALB/c. Bcgr (C.D2) mice, unlike their congenic strain BALB/c, restricted bacterial growth following the intravenous inoculation of 2.5 x 10(8) CFU of M. avium as efficiently as DBA/2 mice. C.D2 and BALB/c peritoneal macrophages from infected mice produced similar amounts of H2O2 but BALB/c mice developed higher levels of NSR to listeria than C.D2 mice. The production of nitrite by peritoneal macrophages from infected mice was found to be enhanced in DBA/2 and C3H/He but not in BALB/c, C57BL/6, DC-1 and C.D2 mice. Resident peritoneal macrophages from C.D2 mice were more bacteriostatic in vitro for M. avium than macrophages from BALB/c mice. The same relative differences between the two macrophage populations were observed when the cells were activated with lymphokines. The results show that the populations were observed when the cells were activated with lymphokines. The results show that the resistance to M. avium infection in mice is under the control of the Bcg gene and that susceptibility may be due to some defect in macrophage antibacterial function not completely overcome by the activation of this phagocyte in the susceptible strains of mice.
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PMID:The role of macrophage activation and of Bcg-encoded macrophage function(s) in the control of Mycobacterium avium infection in mice. 211 16

Although shortly after the onset of a mycobacterial infection granulocytes are present at the site of inflammation, the role of granulocytes in the elimination of mycobacteria is not well understood. In vitro studies with, for example Mycobacterium tuberculosis or M. bovis, are hampered by the slow proliferation and clumping of the bacteria. To avoid these disadvantages, we developed a model using the atypical mycobacterium M. fortuitum. The present study concerned two questions: whether human granulocytes are able to phagocytose and intracellularly kill opsonized M. fortuitum and whether intracellular killing of these bacteria can be enhanced by treatment of the granulocytes with recombinant human interferon-gamma (rIFN-gamma). The results showed that normal granulocytes phagocytosed opsonized M. fortuitum rapidly, but did not kill these bacteria effectively. The intracellular killing of M. fortuitum was significantly enhanced by incubation of the granulocytes with rIFN-gamma for 18 h before the start of the killing assay. Since these rIFN-gamma-pretreated granulocytes did not release more O2- and H2O2 upon stimulation with phorbol 12-myristate 13-acetate or opsonized M. fortuitum than control granulocytes, non-oxidative killing mechanisms are probably involved in the enhanced killing of M. fortuitum.
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PMID:Interferon-gamma-activated human granulocytes kill ingested Mycobacterium fortuitum more efficiently than normal granulocytes. 216 44

The respiratory burst of murine alveolar macrophages (AM) was compared with that of peritoneal macrophages (PM). Superoxide anion (O2-) released from resident AM was similar to that of resident PM. That is, resident AM or PM exposed to phorbol myristate acetate (PMA) released only a small amount of O2-, whereas both macrophages released a large amount of O2- when stimulated with zymosan particles. AM as well as PM obtained from mice injected with Mycobacterium bovis BCG 3 weeks previously (abbreviated to BCG-AM and BCG-PM, respectively) showed an enhanced killing activity to Candida parapsilosis. O2- release of BCG-AM stimulated with zymosan was similar to that of BCG-PM. In both BCG-AM and BCG-PM, maximal O2- response was obtained by stimulation with a lower concentration of zymosan than the concentration which required for resident macrophages to release maximal amount of O2-. There was however, a remarkable difference between the ability of BCG-AM and BCG-PM to release O2- when stimulated with PMA. Markedly enhanced O2- release of BCG-PM was observed. In contrast, O2- release of BCG-AM exposed to PMA was almost the same as that of resident AM. Hydrogen peroxide release of BCG-AM, when stimulated with PMA or zymosan, was compatible with O2- release. Isoquinolinylsulfonyl piperadine (H-7), an inhibitor of protein kinase C, inhibited O2- release of PMA-stimulated BCG-AM and BCG-PM in a dose-dependent manner and the extent of inhibition was greater in O2- release of PM than that of AM. Superoxide anion release in response to zymosan was slightly inhibited by H-7.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Oxygen radical generation of murine alveolar macrophages]. 217 Jul 30

The susceptibilities of Mycobacterium leprae and M. avium complex (MAC) to the H2-O2-Fe-mediated halogenation system supplemented with antimicrobial agents were evaluated by fluorescein diacetate-ethidium bromide (FDA/EB) staining. In the case of M. leprae, the number of greenstained bacteria (intact cells) was reduced in the presence of the H2O2-Fe-mediated halogenation system supplemented with agents possessing antileprosy activity, such as rifampin, 4,4'-diaminodiphenylsulfone (dapsone), clofazimine, and ofloxacin. In the case of the MAC strain, although viable units of the organisms were reduced by the halogenation system alone, the number of greenstained cells in the FDA/EB stain was not reduced, even when the halogenation system was used in combination with ofloxacin. Because stainability of the cells is related to structural and functional intactness of the membrane, differences between M. leprae and the MAC strain imply possible differences in the rigidity of the cell membrane.
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PMID:Susceptibilities of Mycobacterium leprae and M. avium complex to the H2O2-Fe-mediated halogenation system supplemented with antimicrobial agents. 247 23

Two important pathogens of developing countries, Mycobacterium leprae, the etiologic agent of leprosy, and Leishmania donovani, the protozoal parasite that causes kalaazar, persist in the human host primarily in mononuclear phagocytes. The mechanisms by which they survive in these otherwise highly cytocidal cells are presently unknown. Since the best understood cytocidal mechanism of these cells is the oxygen-dependent system that provides lethal oxidants including the superoxide anion (O2-), hydrogen peroxide (H2O2), hydroxyl radical (OH), and singlet oxygen (1O2), we sought specific microbial products of these organisms that might enable them to elude oxidative cytocidal mechanisms. Phenolic glycolipid I of M. leprae and lipophosphoglycan of L. donovani are unique cell-wall-associated glycolipids produced in large amounts by the organisms. In this study, phenolic glycolipid I derivatives and lipophosphoglycan were examined for their ability to scavenge potentially cytocidal oxygen metabolites in vitro. Electron spin resonance and spin-trapping indicate that phenolic glycolipid I derivatives and lipophosphoglycan are highly effective in scavenging hydroxyl radicals and superoxide anions. The results suggest that complex glycolipids and carbohydrates of intracellular pathogens that can scavenge oxygen radicals may contribute to their pathogenicity and virulence.
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PMID:Microbial glycolipids: possible virulence factors that scavenge oxygen radicals. 253 41


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