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)

Mice were infected intravenously with increasing numbers of Mycobacterium habana (simiae serotype II), and the levels of delayed-type hypersensitivity to purified protein derivative and M. habana cytoplasmic protein antigen were determined after 14, 30, and 90 days. A footpad delayed-type hypersensitivity response was seen in 14-day-infected mice and was followed by a persisting anergy. T-cell-enriched suspensions collected 30 and 90 days into the infection (anergic donors) showed depressed transformation indexes after phytohemagglutinin and M. habana cytoplasmic protein antigen treatment in vitro. The corresponding B-cell mitogen (lipopolysaccharide) responses were not affected. Mixing experiments with T-cell-enriched suspensions from day-90 M. habana-infected donors adoptively suppressed lymphocyte transformation by normal and day-14 spleen cells. This effect could be ablated by anti-theta serum and complement treatment of the day-90 cells, indicating that the lack of in vitro responsiveness to cytoplasmic protein antigen was mediated by a population of suppressor T-cells present in the heavily infected spleens. There was no evidence that similar cells were present in the spleens of the 14-day-infected animals. Suppressor T-cells could be induced in vitro by exposure of day-14 spleen cells to concanavalin A or M. habana cytoplasmic protein antigen before they were mixed with normal or day-14 indicator splenic lymphocytes. The timing of the appearance of suppressor T-cells in the infected spleens corresponded to a loss of footpad hypersensitivity by the M. habana-infected animals.
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PMID:Development of suppressor T-cells in Mycobacterium habana-infected mice. 15 68

Antigenic relationships between Mycobacterium vaccae, M. nonchromogenicum, and M. leprae were examined in mice and guinea pigs injected with M. vaccae or M. nonchromogenicum suspensions. The growth of both organisms in outbred ICR and four inbred mouse strains was followed up to 30 days. M. nonchromogenicum persisted in the livers and spleens of the inbred mice substantially better than did the M. vaccae population in the same mouse strains. A translucent colony variant of M. vaccae isolated from the opossum survived in vivo better than the opaque colony isolated from opossums and cattle. Persistence of M. vaccae and M. nonchromogenicum was not markedly increased in T-cell-depleted (nude) mice. Normal mice infected with increasing numbers of M. vaccae did not develop delayed-type hypersensitivity to the homologous M. vaccae cytoplasmic protein antigen. When heat-killed M. vaccae were incorporated into Freund adjuvant, both mice and guinea pigs developed delayed hypersensitivity to cytoplasmic antigens prepared from M. vaccae, M. nonchromogenicum and M. vaccae vaccines cross-sensitized guinea pigs to the M. leprae cytoplasmic antigens.
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PMID:Delayed hypersensitivity responses in mice and guinea pigs to Mycobacterium leprae, Mycobacterium vaccae, and Mycobacterium nonchromogenicum cytoplasmic proteins. 38 13

The association of Mycobacterium leprae with Schwann cells may represent an early crucial step in M. leprae pathogenesis. Using a dissociated Schwann-cell system and anti-mycobacterial monoclonal and polyclonal antibodies directed against surface and cytoplasmic components, we investigated the nature of M. leprae epitopes that mediate cytadhesion. Antibodies to polysaccharide and lipid components of M. leprae cell wall inhibited cytadhesion, whereas those directed against both surface and cytoplasmic protein epitopes did not show any such effect. No synergistic or antagonistic activity in inhibiting cytadhesion was observed when antibodies were used in combination. Thus, the association of M. leprae with Schwann cells may be mediated collectively by more than one of its lipid/polysaccharide epitopes. Also, a role for humoral immunity in intervention in the initial steps of M. leprae pathogenesis needs to be considered.
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PMID:Blocking of Mycobacterium leprae adherence to dissociated Schwann cells by anti-mycobacterial antibodies. 268 36

A decline in 5'-nucleotidase production was observed in short-term tissue culture of guinea pig alveolar, peritoneal, splenic, and liver macrophages during exposure to 10(2) microM rifampicin, 1 microM levamisole, or 10 micrograms of cytoplasmic protein antigen extracted from Mycobacterium microti. Liver macrophage 5'-nucleotidase production was more significantly inhibited by the three agents. Cytoplasmic protein antigen from M. microti was the most potent inhibitor of 5'-nucleotidase production.
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PMID:Effect of rifampin, levamisole, and cytoplasmic protein antigen from Mycobacterium microti on 5'-nucleotidase production by guinea pig macrophages. 628 May 98

Five mycobacterial antigens were compared in an enzyme-linked immunosorbent assay (ELISA) for the serodiagnosis of tuberculosis. The antigens studied were an unheated sterile culture filtrate of Mycobacterium tuberculosis, tuberculin purified protein derivative (PPD) from M. tuberculosis (PPDa), purified cytoplasmic protein antigens 5 and 6 from M. tuberculosis, and a PPD prepared from M. kansasi (PPDk). Multivariate analysis of variance showed that geometric mean titres obtained with each of the antigens in ELISA were significantly different in tuberculosis patients and in control groups. The covariation of the ELISA results with the five antigens was highly interdependent. Analysis of receiver operating characteristics revealed that the most accurate test was obtained with antigen 5. M. tuberculosis PPD, M. tuberculosis antigen 6, and M. tuberculosis culture filtrate were, in descending order, less accurate.
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PMID:Evaluation of mycobacterial antigens in an enzyme-linked immunosorbent assay (ELISA) for the serodiagnosis of tuberculosis. 643 23

Specific pathogen-free B6D2 mice were infected with 10(6) or 10(8) viable Mycobacterium bovis (BCG Pasteur) or Mycobacterium simiae and the in vivo growth curves were correlated with the levels of delayed hypersensitivity developed against a cytoplasmic protein antigen (CPA) injected into a hind footpad at increasing time intervals after infection. Half of the heavily infected, anergic mice were placed on a regimen of 10 mg of rifampin, 5 mg of amikacin and 2 mg of clofazimine per 100 ml of drinking water 2 or 8 weeks into the infection. The number of viable mycobacteria recovered from the lungs and spleens of the treated mice (compared with the corresponding drug-free controls) were reduced by up to 10,000-fold over a 3-month treatment period. Spleen cells were harvested at increasing time intervals from the drug-treated and control mice and T-cell enriched suspensions were tested for blastogenic responsiveness to phytohaemagglutinin (PHA) and to the specific CPA mitogen. The early (day 14) peak in tritiated thymidine ([3H]-TdR) uptake was followed by a sharp drop to near background levels. Cell-mixing experiments demonstrated the presence of a suppressor T-cell population in the heavily infected spleens of the M. simiae-infected mice. The suppressor-cell effect was substantially reduced following combined drug therapy although the specific CPA-mediated response was less affected than the non-specific PHA-mediated response.
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PMID:The effect of combined chemotherapy on suppressor T-cell activity in Mycobacterium simiae-infected mice. 645 54

Specific-pathogen-free B6D2 F1 hybrid mice were infected intravenously with 10(7) to 10(8) viable Mycobacterium kansasii cells. The growth of the five test strains in vivo was correlated with the level of delayed hypersensitivity to a cytoplasmic protein antigen injected into the footpad. M. kansasii TMC no. 1201 and 1203 gave rise to persisting systemic infections with an early delayed hypersensitivity response (day 7) followed by a profound anergy to the cytoplasmic protein antigen injections. Strains 1204, 1214, and 1217 declined in viability relatively rapidly and failed to induce detectable levels of delayed hypersensitivity. Spleens harvested from mice infected 20 to 30 days earlier with 10(8) M. kansasii 1203 cells contained a T-cell subpopulation capable of suppressing mixed lymphocyte reactions between normal B6D2 and C3H(He) cells. On the other hand, splenic T-cells taken from M. kansasii 1214-infected mice enhanced, rather than suppressed, the indicator mixed lymphocyte reactions. The kinetics of stimulator-suppressor T-cell production within the spleens of the heavily infected mice differed as the two contrasting M. kansasii infections progressed. Such cellular interactions could well be responsible for the observed persistence of the systemic M. kansasii 1203 infection.
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PMID:Systemic Mycobacterium kansasii infection and regulation of the alloantigenic response. 645 61

Various species of atypical mycobacteria exhibited a wide range of growth patterns in the lung, liver, and spleen of specific pathogen-free B6D2 mice infected with these organisms. The growth varied from rapid elimination (complete avirulence) to a continued persistence in the lung, which eventually resulted in the death of many of the mice. Prior depletion of the T cells of aerogenically challenged mice did not affect the growth characteristics of the organisms within the lungs. Mice infected with Mycobacterium habana developed an early hypersensitivity response to the cytoplasmic protein antigens (CPA) of this organism, and this response was followed by a persistent state of anergy. Mice infected with Mycobacterium simiae failed to develop detectable levels of hypersensitivity at any time during the study. Spleen cells taken from mice infected with M. habana or M. simiae exhibited an early peak in the incorporation of [3H] thymidine after exposure of the cells to the nonspecific T-cell mitogen phytohemagglutinin (PHA). A similar peak occurred when the cells were exposed to the specific mitogen CPA of M. habana. Later in the infection, the anergic spleen cells showed no transformation of lymphocytes after exposure to either PHA or CPA. T-cell-mixing experiments, which were carried out both before and after treatment of suspensions of cells from the anergic spleens with anti-Thy 1.2 antiserum plus complement, indicated the presence of a population of suppressor T cells in the anergic animals.
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PMID:Immune responses to atypical mycobacterial lung infections. 646 12

In this study, we evaluated vaccination with a number of purified, as well as recombinant, Mycobacterium leprae proteins for protective efficacy in mice. BALB/c mice were immunized intradermally with various native somatic (purified) or recombinant M. leprae proteins and their synthetic polypeptides emulsified in Freund's incomplete adjuvant. The protective efficacy of these preparations was assessed by enumeration of bacilli in the footpads of mice challenged with viable M. leprae 1 to 2 months following immunization. Protection was afforded by the purified and recombinant 10-kDa M. leprae cytoplasmic heat shock protein, the recombinant cell wall-associated 65-kDa M. leprae heat shock protein, and to a lesser extent, the purified 28-kDa M. leprae cytoplasmic protein (superoxide dismutase). Vaccination with either the purified or recombinant 35-kDa M. leprae cell membrane protein, the synthetic 27-amino-acid N-terminal peptide of the 10-kDa protein, the recombinant 18-kDa M. leprae protein, or the purified 22-kDa cell membrane protein was ineffective. When the interval between immunization and challenge was increased to 6 months, the purified 10-kDa M. leprae protein and the recombinant 65-kDa M. leprae protein lost vaccine efficacy, while a sodium dodecyl sulfate-soluble protein fraction of the M. leprae cell wall (soluble proteins), as had been found previously, continued to protect, suggesting that multiple M. leprae protein epitopes are critical for solid vaccine protection.
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PMID:Vaccination with pure Mycobacterium leprae proteins inhibits M. leprae multiplication in mouse footpads. 792 81

This review compares the clinical usefulness of immunological methods for the detection of structural components and metabolites of bacteria and fungi. Bacterial antigens (especially those of Mycobacterium, Neisseria, Staphylococcus aureus, Yersinia enterocolitica, Escherichia coli, Salmonella, Chlamydia, and Brucella) are best detected by enzyme-linked immunosorbent assay. Methods involving antibodies are more expensive and are effective only when performed in series. The detection of antibodies that recognize S aureus teichoic acid merely confirms the presence of a metastatic complication. Tissue invasion by Candida albicans is not yet reliably detectable by the presence of a specific antigen. Simple, but not completely reliable methods are available such as the latex test for mannans detection and/or agglutination with liposomes for detecting 48-kDa cytoplasmic protein antigen and an assay for detecting enolase antigen. A latex agglutination test has also been developed for the mannans antigen of Aspergillus and for Cryptococcus neoformans capsular polysaccharide; the latter test is more cost effective. The sensitivity of both tests is improved by serial assays. A negative finding with hemagglutination-based antibody tests rules out C albicans infection, and titers of 1/640 or higher have been associated with disseminated infection by Aspergillus. Concentrations of C albicans blastopore antigen antibodies higher than 400 IU/ml can be seen in disseminated candidiasis. High concentrations of endotoxin are indicative of imminent septic shock. Some biological indicators (C reactive protein, angiotensin converting enzyme, fibronectin, elastase-alpha 1-antitrypsin complex, tumor necrosis factor and interleukin-6) have been used to rule out a bacterial cause of fever.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunological methods for the detection of structural components and metabolites of bacteria and fungi in blood. 821 14


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