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

Comparisons were made of the yield, chemical content, and biological activity of filtrates and extracts obtained by sonic and pressure cell disruption of bacilli from 4- and 8-week-old Proskauer and Beck cultures of the H37Rv strain (TMC no. 102) of Mycobacterium tuberculosis. The culture filtrates were dialyzed, freeze-dried, reconstituted in saline, and sterilized by membrane filtration. The viable bacilli were washed and resuspended in distilled water and subsequently disrupted either by sonication in the cold for 15 or 30 min or by treatment at 20,000 or 40,000 lb/in2 in a pressure cell. The resulting extracts were clarified by centrifugation, concentrated, and sterilized by filtration. All preparations were adjusted to contain 10 mg of solids (dry weight)/ml and were analyzed quantitatively for protein, deoxyribonucleic acid, ribonucleic acid, polysaccharide, and lipid content. Separation patterns obtained by gradient acrylamide gel electrophoresis, as well as by one- and two-dimensional immunoelectrophoresis, provided the basis for qualitative comparisons of the culture filtrates and cell extracts. Three-point dose-response curves also were used to compare the preparations for skin test reactivity in BCG-vaccinated guinea pigs. It was concluded that, although there were no consistent differences in chemical content or biological activity between the preparations, a 15-min sonic treatment appeared to be the most suitable method for preparation of bacillary extracts based on yield of active components and ease of preparation.
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PMID:Comparison of antigens in sonic and pressure cell extracts of Mycobacterium tuberculosis. 81 43

In Mycobacterium phlei TMC 1548 supplementation of growth medium containing 2% v/v glycerol with glucose (up to 5% w/v) resulted in an increase in growth (yield of cells), in amount of total phospholipids, and in each of the individual phospholipids (cardiolipin, phosphatidylethanolamine, phosphatidylinositol and its mannosides, and phosphatidylglycerol). However, when the medium was supplemented with a higher concentration (7.5% w/v) of glucose, both growth and phospholipid levels decreased to near control values (2% v/v glycerol alone). Cyclic AMP levels, which decreased at all concentrations of glucose, had no relation to phospholipid content or growth. The presence of a protein that possesses the property of stimulating c-AMP phosphodiesterase activity was recently demonstrated in Mycobacterium smegmatis (Falah et al. 1988. FEMS Microbiol. Lett. 56: 89-93). In M. phlei the level of this calmodulin-like protein (assayed by radioimmunoassay) changed with different concentrations of glucose in the growth medium in a manner identical with that of phospholipids. We suggest that in mycobacteria (i) intracellular calmodulin-like protein levels are affected by glucose concentration in the growth medium and (ii) there is a positive correlation between the levels of calmodulin-like protein, total and individual phospholipids, and growth (yield of cells) in glucose-grown M. phlei.
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PMID:Correlation between calmodulin-like protein, phospholipids, and growth in glucose-grown Mycobacterium phlei. 131 78

A DNA probe specific for Mycobacterium kansasii was obtained from a plasmid clone library of EcoRI-digested genomic DNA. The probe specifically identified culture-confirmed isolates of M. kansasii and isolates in cultures of environmental water samples. In an attempt to distinguish between isolates of M. kansasii, we used two methods to demonstrate restriction fragment length polymorphisms in the genomic DNA. Both of these methods failed to detect any differences between the isolates. These isolates included the type strain TMC 1201, environmental isolates, and clinical isolates from Australia and the Solomon Islands. This result suggests that the genome of M. kansasii is highly conserved and that genetic divergence within this species in insignificant.
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PMID:Identification of Mycobacterium kansasii by DNA hybridization. 168 42

Mouse T cell clones against live Mycobacterium avium were generated from the spleens of BALB/c mice infected with M. avium TMC 702. Eighth clones were of the L3T4+ subset, whereas two were of Lyt2+ subset. Six of the L3T4+ T cell clones were of the TH1 subset whereas two were of the TH2 subset, judged on the profile of cytokine release. One of the Lyt2+ clones exhibited significant cytotoxicity against M. avium-infected mouse macrophages. Transfer of clones to nude BALB/c mice infected with M. avium was associated with insignificant changes in resistance for seven clones. One clone, of the L3T4+/TH2 subset, transferred significant resistance to the infection, also associated with infusion of supernatants from the clone, which was fully inhibited by neutralizing with anti-interleukin 4. By contrast, infusion of one TH1 clone and the cytolytic Lyt2+ led to increased microbial growth in the spleens and livers of infected mice, which was not apparent on infusion with supernatants. Application of clones' supernatants on infected macrophages had marginal effects on M. avium growth and was not correlated with protective or suppressive activity. Overall, these results suggest that T cells may influence M. avium growth in vivo in a bidirectional manner and also suggest that interleukin 4 may be an important factor in host resistance to M. avium.
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PMID:Mouse T cell clones against Mycobacterium avium: identification of clones that modify resistance against atypical mycobacteria infection. 174 Jun 47

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

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

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

Growth of the virulent Mycobacterium avium strain TMC 724 in host tissues during persistent infection of mice was studied. Following intravenous infection of C57BL/6 mice, the kinetics of bacterial growth was biphasic in the spleen and liver, with a significant reduction of the multiplication rate after day 21 to 28 of infection. An electron-microscopic study of the liver and spleen of infected mice showed that the bacteria were strictly intracellular. They were observed within inflammatory macrophages populating granulomas disseminated in host tissues. The bacteria were confined to the phagosome compartment, and they were encapsulated. Phagosome-lysosome fusions were encountered, but the bacteria showed no visible signs of degradation and continued to multiply. These results are the first in vivo evidence that virulent M. avium multiplies exclusively intracellularly and that encapsulated bacteria resist the microbicidal mechanisms of macrophages inside the phagosomal compartment.
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PMID:Intramacrophage growth of Mycobacterium avium during infection of mice. 203 82

Intradermal immunization with killed Mycobacterium leprae renders mice immune to infection with viable M. leprae. This protection is long lasting and systemic in that immunization in the left flank results in protection in both the left and right footpads. Immunization with Mycobacterium vaccae was ineffective in protecting mice against M. leprae infection, while Mycobacterium bovis BCG provided partial protection. Mycobacterium habana TMC 5135 (now known as Mycobacterium simiae) was found to be as effective as M. leprae in protecting mice against footpad infection.
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PMID:Vaccination of mice against Mycobacterium leprae infection. 264 81

Arginine decarboxylase (arginine carboxy-lyase, EC 4.1.1.19) from Mycobacterium smegmatis, TMC 1546 has been purified to homogeneity. The enzyme has a molecular mass of 232 kDa and a subunit mass of 58.9 kDa. The enzyme from mycobacteria is totally dependent on pyridoxal 5'-phosphate for its activity at its optimal pH and, unlike that from Escherichia coli, Mg2+ does not play an active role in the enzyme conformation. The enzyme is specific for arginine (Km = 1.6 mM). The holoenzyme is completely resolved in dialysis against hydroxylamine. Reconstitution of the apoenzyme with pyridoxal 5'-phosphate shows sigmoidal binding characteristics at pH 8.4 with a Hill coefficient of 2.77, whereas at pH 6.2 the binding is hyperbolic in nature. The kinetics of reconstitution at pH 8.4 are apparently sigmoidal, indicating the occurrence of two binding types of differing strengths. A low-affinity (Kd = 22.5 microM) binding to apoenzyme at high pyridoxal 5'-phosphate concentrations and a high-affinity (Kd = 3.0 microM) binding to apoenzyme at high pyridoxal 5'-phosphate concentrations. The restoration of full activity occurred in parallel with the tight binding (high affinity) of pyridoxal 5'-phosphate to the apoenzyme. Along with these characteristics, spectral analyses of holoenzyme and apoenzyme at pH 8.4 and pH 6.2 indicate a pH-dependent modulation of coenzyme function. Based on the pH-dependent changes in the polarity of the active-site environment, pyridoxal 5'-phosphate forms different Schiff-base tautomers at pH 8.4 and pH 6.2 with absorption maxima at 415 nm and 333 nm, respectively. These separate forms of Schiff-base confer different catalytic efficiencies to the enzyme.
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PMID:Modulation of arginine decarboxylase activity from Mycobacterium smegmatis. Evidence for pyridoxal-5'-phosphate-mediated conformational changes in the enzyme. 266 97


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