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)

Twenty cases of tuberculous meningitis were diagnosed at the Hamad Medical Corporation between 1990 and 1995. Most of the patients (90%) were expatriates. The most common presenting features were fever, headache, neck stiffness and altered mental status. Five patients were in stage 1 disease at the time of presentation, 11 in stage 2, and four in stage 3. Examination of cerebrospinal fluid showed at least one abnormal finding in all patients, and culture grew Mycobacterium tuberculosis in 50%. A positive tuberculin skin test in 50% of patients, abnormal chest X-ray in 35%, abnormal CT scan or MRI showing tuberculoma or hydrocephalus in 55%, and positive sputum culture for M. tuberculosis in 15% helped establish the diagnosis. All the patients were treated with antituberculous drugs and steroids. Seventeen (85%) survived, three with severe neurological sequelae; three (15%) died. Poor outcome was associated with advanced stage of disease at presentation and high CSF protein. Tuberculous meningitis continues to be an important disease in Qatar, especially in expatriates, and should be considered in the differential diagnosis in any patient presenting with fever and change in sensorium.
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PMID:Tuberculous meningitis: a clinical and laboratory study of 20 patients in Qatar. 979 60

A 10-month-old infant with tuberculous (Tb) meningitis accompanying hydrocephalus was successfully treated with a VP shunt operation soon after a PCR assay of CSF was found to be negative for Mycobacterium tuberculosis. PCR assay of CSF is helpful for determination of the timing for VP shunting in Tb meningitis.
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PMID:Tuberculous meningitis with hydrocephalus. Contribution of PCR assay of CSF before VP shunting. 984 Mar 62

Macrophage inhibitory factor-A3 (MIF-A3) is a fraction derived from Mycobacterium avium serovar 2 (Mav2) that consists of a small amine containing compound (peptide), trehalose and two or three short chain fatty acids. MIF-A3 has been shown to inhibit candidacidal activity of murine thioglycolate-elicited peritoneal-derived macrophages and bovine peripheral blood monocytes, and scavenge reactive oxygen intermediates. In this study, MIF-A3 was evaluated for its effect on secretion of IL-1beta, IL-6, IL-10, TNFalpha and GM-CSF in C57BL/6 murine thioglycolate-elicited peritoneal-derived macrophages, with and without pre-incubation with affinity purified goat anti-MIF-A3 IgG, using ELISA cytokine kit analysis. Results of this study suggest that anti-MIF-A3 IgG does not enhance clearance of Mav2, alter phagocytosis or alter phagosome-lysosome interactions as determined by electron microscopy in Mav2 infected macrophages. MIF-A3 does induce secretion of IL-6, but does not induce secretion of TNFalpha, IL-1beta, and GM-CSF. TNFalpha has been previously shown to reduce growth, while IL-6 has been shown to enhance growth of M. avium. Since IL-6 appears to enhance growth of M. avium and MIF-A3 induces IL-6 secretion, MIF-A3 may be responsible for enhanced intracellular growth in M. avium infections and be a factor in the pathogenesis of M. avium infections.
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PMID:Effects of macrophage inhibitory factor-A3 (MIF-A3) on cytokine secretion and phagolysosome fusion in murine macrophages. 1006 27

In this study, 30 AIDS patients without Mycobacterium avium infection were randomized to receive treatment with azithromycin (1200 mg), granulocyte-monocyte colony-stimulating factor (GM-CSF; 250 microg/m2/day for 5 days), or both agents. The M. avium killing capacity of neutrophils and monocytes harvested from each patient before intervention and during (day 4), and after therapy (day 8) was assessed. The mean virus load change in the groups receiving GM-CSF was +0.14 log human immunodeficiency virus RNA. After GM-CSF therapy, neither neutrophils nor monocytes could significantly reduce M. avium growth (P=.96 and.31, respectively). Bone pain, myalgia, presyncope, or fever occurred in 55% of patients receiving GM-CSF. Thus, the GM-CSF regimen used in this study did not affect virus load, frequently caused adverse reactions, and did not improve the M. avium killing capacity of neutrophils and monocytes. Future studies using a different GM-CSF regimen are indicated.
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PMID:Killing of Mycobacterium avium by neutrophils and monocytes from AIDS patients treated with recombinant granulocyte-macrophage colony-stimulating factor. 1035 87

Dendritic cells (DC) are powerful antigen presenting cells, which have the unique capacity to stimulate naive T cells. In spite of the well-known decline of T cell function in old age, little information is available on whether DC are also affected by the aging process. This is mainly due to problems with the isolation and purification of DC. Rapid progress in the characterization of DC has been made in recent years, as simple methods to generate large numbers of DC from precursors have been developed. It was the aim of the present study to compare monocyte derived DC from old and young healthy persons. The generation of DC from blood monocytes in response to GM-CSF and IL-4 treatment was similar in cells from young and old persons. The DC population thus obtained had a typical dendritic morphology and expressed DC surface markers, such as HLA class II, CD1a, CD11c, CD54, CD80 and CD86, but not CD14 for a period of up to three weeks in culture. DC from young and old persons produced IL-12 and TNF-alpha and responded equally well to maturation-inducing stimuli. DC maturation was stimulated by purified protein derivative (PPD) of Mycobacterium tuberculosis, whole inactivated influenza virus and by influenza split vaccine, but not by purified viral RNA. When tested for their antigen-presenting capacity, DC from young and old persons were capable of stimulating the proliferation and the cytokine production of T cells. It was of particular interest that CD45RA(+) as well as CD45RO(+) T cells from aged donors were unable to respond to stimulation with influenza proteins presented by monocytes, but were triggered to proliferate and to produce cytokines when antigen was presented by DC. The results demonstrate that DC from old persons (a) may still function as powerful antigen-presenting cells provided the right differentiation and maturation stimuli are present; (b) are capable of mobilizing residual capacity in senescent T cells and (c) may therefore represent a potent tool for immunotherapy and vaccines in old age.
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PMID:Unimpaired dendritic cells can be derived from monocytes in old age and can mobilize residual function in senescent T cells. 1068 36

To generate an in vivo system for investigating the postintegration phase of HIV-1 replication, mouse lines transgenic for a full-length infectious proviral clone of a monocyte-tropic HIV-1 isolate, HIV-1JR-CSF, were constructed. Leukocytes from two independent JR-CSF transgenic mouse lines produced HIV-1 that infected human PBMCs. Plasma viremia was detected in these mice at levels (mean, >60,000 HIV RNA copies/ml) comparable to those reported for HIV-1-infected individuals. The levels of HIV RNA in these mice increased several-fold after either treatment with the superantigen Staphylococcus enterotoxin B or infection with Mycobacterium tuberculosis. Thus, a provirus encoding a monocyte-tropic HIV-1 strain under the control of its LTR expressed as a transgene in mice can proceed through the postintegration replication phase and produce infectious virus. In addition, the presence of plasma viremia that can be monitored by measuring plasma HIV-1 RNA levels permits these mice to be used to study the impact of different interventions on modulating in vivo HIV-1 production. Therefore, these mice provide a novel manipulable system to investigate the in vivo regulation of HIV-1 production by factors that activate the immune system. Furthermore, this murine system should be useful in delineating the role of human-specific factors in modulating HIV-1 replication and investigating the in vivo therapeutic efficacy of agents that target the postintegration stages of HIV-1 replication.
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PMID:Mice transgenic for monocyte-tropic HIV type 1 produce infectious virus and display plasma viremia: a new in vivo system for studying the postintegration phase of HIV replication. 1077 34

Both the CD4-CD8- (double negative) and CD4-CD8+ T cell lineages have been shown to contain T cells which recognize microbial lipid and glycolipid Ags in the context of human CD1 molecules. To determine whether T cells expressing the CD4 coreceptor could recognize Ag in the context of CD1, we derived CD4+ T cell lines from the lesions of leprosy patients. We identified three CD4+ Mycobacterium leprae-reactive, CD1-restricted T cell lines: two CD1b restricted and one CD1c restricted. These T cell lines recognize mycobacterial Ags, one of which has not been previously described for CD1-restricted T cells. The response of CD4+ CD1-restricted T cells, unlike MHC class II-restricted T cells, was not inhibited by anti-CD4 mAb, suggesting that the CD4 coreceptor does not impact positive or negative selection of CD1-restricted T cells. The CD4+ CD1-restricted T cell lines produced IFN-gamma and GM-CSF, the Th1 pattern of cytokines required for cell-mediated immunity against intracellular pathogens, but no detectable IL-4. The existence of CD4+ CD1-restricted T cells that produce a Th1 cytokine pattern suggests a contributory role in immunity to mycobacterial infection.
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PMID:Evidence for human CD4+ T cells in the CD1-restricted repertoire: derivation of mycobacteria-reactive T cells from leprosy lesions. 1077 86

The interaction of various pathogenic (Mycobacterium tuberculosis, M. avium, M. kansasii, M. xenopi), and non-pathogenic mycobacteria (M. smegmatis, M. phlei) with human macrophages at the level of macrophage cytokine expression (TNFalpha, IL1, IL6 and GM-CSF) was investigated. Both for TNFalpha and GM-CSF, the lowest levels were obtained with pathogenic mycobacterial species, whereas about 2-8 times higher levels were observed for non-pathogenic species. Contrary to the above, the differences for IL6 and IL1 were not marked, although IL6 appeared to be more elevated for non-pathogenic species. Heat-killed bacteria induced a lower level of the cytokines for all the three cytokines assayed (TNFalpha, IL6 and IL1), except for M. tuberculosis for whom a significantly higher proportion of TNFalpha was induced by killed bacilli. The RT-PCR experiments performed on M. avium (as a low inducer of the cytokines) and M. smegmatis (as a high inducer of the cytokines) showed that the differences observed among pathogenic vs non-pathogenic strains were also reflected at the transcriptional level for TNFalpha and to a lesser extent for IL6, but not for IL1. This investigation underlined important differences existing between the pathogenic and non-pathogenic species, particularly as regards TNFalpha and GM-CSF.
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PMID:Secretion of cytokines by human macrophages upon infection by pathogenic and non-pathogenic mycobacteria. 1079 81

Various bacterial cell wall components have been shown to induce hyporesponsiveness in macrophages (MAC). Here, mycobacterial glycolipids were employed to determine whether they induce a state of 'tolerance/hyporesponsiveness' in MAC in vitro in order to assess whether mycobacterial components negatively affect the immune response to Mycobacterium tuberculosis. Arabinosylated lipoarabinomannan (ARA-LAM) stimulated hyporesponsiveness by reducing TNF-alpha, GM-CSF, G-CSF, IL-10, and IL-6 release similarly to LPS, but caused no changes in IL-8 secretion. Mannose-capped LAM (MAN-LAM) acted in a different way in that TNF-alpha, GM-CSF, and IL-10 were upregulated after restimulation of MAC. Blocking experiments by mannan suggest mannose-receptor involvement in MAN-LAM activation only. Cross-stimulation experiments demonstrated a hierarchy of signaling, with LPS being the most potent stimulator and mediating abrogation of ARA-LAM-stimulated tolerance but not vice versa. MAN-LAM was the least potent stimulator of either MAC activation and induction of hyporesponsiveness. Similarly to LPS, ARA-LAM upregulated CD14 surface expression after restimulation. Recurrent MAN-LAM treatment either downmodulated or did not induce any change in CD14 expression. The role of MAN-LAM regulated cytokine secretion as well as implications regarding M. tuberculosis infection will be discussed.
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PMID:Differential tolerance induction by lipoarabinomannan and lipopolysaccharide in human macrophages. 1086 91

Recent studies have implicated Toll-like receptors (TLR), especially TLR2 and TLR4, as sentinel receptors that signal the interaction of macrophages with bacterial pathogens via a NF-kappaB-mediated pathway. The regulation of TLR gene expression, however, has not been intensively studied. Here, we report that TLR2 mRNA was induced following infection of murine macrophages with Mycobacterium avium. The changes in TLR2 mRNA correlated with an increase in TLR2 surface expression. Infection with M. avium resulted in a concomitant decrease in TLR4 mRNA. The effect of M. avium infection on TLR2 mRNA appeared to be mediated, in part, by TLR2 because the induction of the mRNA was partially blocked by preincubation of the macrophages with an anti-human TLR2 Ab. In contrast, the effect of LPS stimulation was mediated via TLR4 because infection of macrophages from LPS(d) mice, which do not express active TLR4, resulted in an increase in TLR2 mRNA, while treatment of macrophages from these mice with LPS failed to induce TLR2 mRNA. Several cytokines, including TNF-alpha, IL-1alpha, and GM-CSF, but not IFN-gamma, induced TLR2 mRNA. M. avium infection resulted in the induction of TLR2 mRNA by macrophages from both TNFRI knockout and NF-kappaB p50 knockout mice.
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PMID:Regulation of toll-like receptor 2 expression by macrophages following Mycobacterium avium infection. 1108 67


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