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

A patient with pulmonary tuberculosis caused by bacteria resistant to various anti-microbial agents was treated with adoptively transferred autologous peripheral blood leucocytes (PBL) sensitized with killed Mycobacterium tuberculosis organisms in vitro. The 32-year-old man was admitted to our hospital from National Sanitarium Okinawa Hospital with weight loss, high fever, and rapid aggravation on chest X-ray. Patient's PBL obtained by leukapheresis and separated with Ficoll-Hypaque solution were cultured with killed Mycobacterium tuberculosis bacteria of 0.4 microgram per ml at 1 x 10(6) cells per ml for 7 days in media containing 0.5 U recombinant 1L-2 per ml. After incubation, PBL were layered and centrifuged on Ficoll-Hypaque solution and washed three times with saline. PBL (1-3 x 10(8)) were combined and concentrated for infusion in 20 to 30 ml saline. After injection, patient displayed fever and transitory drop of PaO2. Although the patient did not have an improved on chest X-ray, his fever was alleviated, weight was increased, accelerated ESR was slightly improved, and the number of organisms in sputum (Number of Gaffky) temporarily decreased. Adoptive immunotherapy using the autologous PBL which were sensitized with killed bacteria may be an effective anti-tuberculous immunotherapy.
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PMID:[Adoptive immunotherapy for pulmonary tuberculosis caused by multi-resistant bacteria using autologous peripheral blood leucocytes sensitized with killed Mycobacterium tuberculosis bacteria]. 194 28

Doses of as little as 50 micrograms of a soluble chaotropic extract of bovine tubular basement membrane (Bov-KBr-TBM) with adjuvants induced anti-TBM antibodies and tubulointerstitial nephritis (TIN) in Brown Norway (BN) rats. The lesion was shown by renal histology, by deposition of IgG and C3 along TBM, and in terms of the humoral and cellular immune responses to compare to that produced by the standard immunization (particulate bovine TBM) for this model of TIN in BN rats. More than half of the mononuclear cells in kidneys of BN rats with TIN bore various T-cell antigens (monoclonal antibodies W3-13, W3-25, and OX-8), and most of the infiltrating cells were positive for Ia (monoclonal antibody OX-6) by indirect immunofluorescence. Purified suspensions of these mononuclear infiltrates were prepared by using Ficoll-Hypaque gradients and the fluorescence-activated cell sorter (FACS) to eliminate renal tubular epithelial cells. The purified mononuclear cells, cultured for 5 days, incorporated thymidine in response to concanavalin A (Con A), Mycobacterium tuberculosis purified protein derivative, and Bov-KBr-TBM but not in response to a variety of autologous renal antigens. After culture for 5 days in Bov-KBr-TBM and Con A supernatant, lymph node cells (LNC) from Bov-KBr-TBM-immunized BN rats passively transferred TIN to naive BN rats. Although no cells reactive with autologous renal antigens were detected in the renal infiltrates, the transfer of disease with propagated LNC suggests that elements of the cellular immune system, in addition to anti-TBM antibody, contribute to the generation of this BN-TIN.
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PMID:Tubulointerstitial nephritis induced in the brown Norway rat with chaotropically solubilized bovine tubular basement membrane: the model and the humoral and cellular responses. 400 24

We describe a rapid polymerase chain reaction (PCR)-based test for diagnosing Mycobacterium avium directly from blood specimens. Blood was collected in anticoagulant (EDTA) from patients who also had blood cultures performed by the lysis-centrifugation method. Blood samples were centrifuged on a Ficoll-Hypaque gradient to purify peripheral blood mononuclear cells. The purified cells were washed and incubated in the presence of Chelex-100 (a divalent cation-binding resin), boiled to release mycobacterial DNA, and then amplified with M. avium-specific PCR primers. Amplification was detected by hybridization with radiolabelled probe, and the results were compared with the culture results. The PCR assay gave positive results for 12 of 15 specimens that were taken from patients with positive cultures for M. avium complex (sensitivity, 80%). The three PCR-negative specimens in this group showed evidence of PCR inhibition. The PCR assay gave positive results for 32 of 228 specimens taken from patients with negative cultures (specificity, 86%). Of these 32 PCR-positive culture-negative specimens, 27 were also positive when amplified with primers specific for the genus Mycobacterium, suggesting that PCR may be more sensitive than culture.
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PMID:Diagnosis of Mycobacterium avium bacteremia by polymerase chain reaction. 834 58

One hundred fifty-three blood samples from patients positive for the human immunodeficiency virus (HIV) were analyzed by polymerase chain reaction (PCR) to detect the presence of Mycobacterium avium. Samples were collected from patients who also had blood cultures performed by a radiometric method. Blood samples were centrifuged on a Ficoll-Hypaque gradient to purify peripheral blood mononuclear cells. The purified cells were washed and incubated with a resin, boiled to release mycobacterial DNA, and then amplified. Polymerase chain reaction products were detected by a nonisotopic method. A 123 base-pair (bp) insertion sequence, namely IS6110, from Mycobacterium tuberculosis complex was also included in the reaction as an internal control of Taq polymerase activity to exclude the presence of enzyme inhibitors. This IS6110 fragment can be distinguished from the 383 bp target product on ethidium bromide-stained agarose gel and may also be used in a colorimetric assay. Such results were compared with the results of culture and indicated that the assay is as sensitive as bacteriological methods, though faster.
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PMID:Detection and identification of Mycobacterium avium in the blood of AIDS patients by the polymerase chain reaction. 887 71

Mycobacterium avium-intracellulare (MAI) is a ubiquitous environmental pathogen that causes disseminated infection in immunocompromised patients, such as those with human immunodeficiency virus, interleukin-12 deficiency, or interferon-gamma receptor mutation. Colony morphotypes are associated with MAI pathogenicity. Our previous studies have reported that smooth-transparent (SmT) morphotypes are more virulent and induce less cytokine (interleukin-1beta and tumor necrosis factor-alpha) production by human monocytes than the smooth-domed (SmD) morphotypes. Mitogen-activated protein (MAP) kinases such as extracellular-regulated kinase (ERK) are activated by the phagocytosis of particle antigens in macrophages, and this ERK activation subsequently influences cytokine expression and the control of intracellular pathogen growth. The influence of MAP kinase activation on MAI replication in human monocytes was examined. Peripheral blood monocytes isolated from healthy subjects by Ficoll-Hypaque sedimentation were infected with virulent SmT or avirulent SmD MAI without or with MAP kinase inhibitors. MAP kinase activities were determined by in vitro kinase assay, intracellular MAI growth by CFU assay, and cytokines by enzyme-linked immunosorbent assay. MAI infection induced ERK and p38 activation. Inhibition of ERK by PD98059, but not p38, significantly increased intracellular MAI growth. Tumor necrosis factor-alpha release and interleukin-1beta production in response to MAI were reduced by MAP kinase inhibition. p38 inhibition tended to reduce cytokine production more substantially. These data suggest that ERK activation limits intra-monocytic MAI replication and enhances monocytic cytokine release, whereas p38 activation influences only cytokine release. The effect of MAP kinases on MAI growth might thus be mediated by the modulation of cytokine production.
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PMID:Extracellular-regulated kinase activation regulates replication of Mycobacterium avium intracellularly in primary human monocytes. 1833 41