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)

Tuberculin PPD and PPD-Battey skin tests were simultaneously applied to 3,882 employees of Charity Hospital and 408 medical students at Louisiana State University. The PPD was doubtful (5 to 9 mm induration) in 253 of the total 4,290 persons tested (5.9%). In 86 of these 253 persons, the reaction to PDD-Battey was greater than the reaction to PPD, presumably identifying a subpopulation with a falsely positive PPD and therefore at considerably lower risk of developing future tuberculous disease. Of the 408 medical students (average age 24 years), 80 (19.6%) were classified by the skin tests as having atypical mycobacterial sensitization as compared to six (1.45%) who were classified positive or probably positive to Mycobacterium tuberculosis (P less than .001). In the Southeastern United States, where the incidence of atypical mycobacterial infection is relatively high and occurs at a young age, dual skin testing may have its greatest applicability in identifying tuberculous infection when the PPD falls in the "doubtful" 5 to 9 mm range.
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PMID:PPD-tuberculin and PPD-Battey dual skin testing of hospital employees and medical students. 68 72

TGF-beta at 1 and 10 ng/ml inhibited H2O2 production and fibronectin adherence by human monocytes. Coculture with anti-TGF-beta Abs or with IFN-gamma, but not with growth hormone, abrogated these effects. Neither viability nor superoxide production were decreased by TGF-beta treatment. TGF-beta appeared to be inhibiting H2O2 production rather than inducing catalase as preincubation in azide was without effect. Also, TGF-beta did not inhibit activity against virulent Mycobacterium tuberculosis. Coculture of monocytes with IFN-gamma + TGF-beta in vitro moderately inhibited the growth of M. tuberculosis when compared with untreated cells. Phagocytosis was not inhibited. Treatment of monocytes with another combination of cytokines, IFN-gamma+ TNF-alpha + vitamin D3, markedly reduced bacterial viability, although this appeared to be due to decreased phagocytosis leading to extracellular death of the bacteria. We conclude that despite suppressing some monocyte functions such as H2O2 production and adherence, TGF-beta, in combination with other cytokines, leaves other antimicrobial functions of the monocyte unaffected or even enhanced.
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PMID:Selective deactivation of human monocyte functions by TGF-beta. 767 31

We examined the ability of purified protein derivative (PPD) of Mycobacterium tuberculosis to induce transforming growth factor beta 1 (TGF-beta 1), a potent immunosuppressive and macrophage-deactivating molecule, in blood monocytes from healthy individuals. TBF-beta 1 activity in PPD-induced monocyte supernatants was identified by Western immunoblot analysis and was not inhibited by polymyxin B, an inhibitor of bacterial lipopolysaccharide (LPS). Furthermore, PPD at equivalent amounts in weight to LPS was as potent in stimulation of monocyte production of TGF-beta 1 at 24 h of culture, as quantified by enzyme-linked immunosorbent assay. The inducing effect of PPD, in contrast to that of LPS, was sustained at later time points of culture (72 h). PPD enhanced the constitutive expression of TGF-beta 1 steady-state mRNA in monocytes at 24 and 48 h of culture. In contrast, neither mycobacterial heat shock protein (64-kDa protein of M.bovis) nor LPS induced TGF-beta 1 mRNA. Decay studies suggested a transcriptional rather than a posttranscriptional effect of PPD on TGF-beta 1 gene expression.
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PMID:Induction of transforming growth factor beta 1 by purified protein derivative of Mycobacterium tuberculosis. 780 61

Transforming growth factor-beta 1 (TGF-beta 1) is a potent immunoregulatory molecule. It modulates production of cytokines, such as TNF-alpha and IL-6, and cell response to cytokine stimulation. Mycobacterium avium is an intracellular bacterium that multiplies within macrophages. The reason why M. avium can survive within macrophages is still unknown but probably is multifactorial. Exposure of M. avium-infected macrophages to rTGF-beta 1 before TNF stimulation significantly decreases the mycobactericidal/mycobacteriostatic activity associated with treatment with TNF. Infection of human monocyte-derived macrophages in vitro with M. avium strains belonging to serovars 1, 4, and 8 induced secretion of biologically active TGF-beta. The production of TGF-beta was strain dependent and was more pronounced in macrophages infected with virulent strains. Incubation of macrophages with M. avium-derived 33-kDa and 65-kDa proteins was associated with significant release of biologically active TGF-beta. Treatment of M. avium-infected macrophages with rTNF-alpha in the presence of anti-TGF-beta 1 antibody induced significantly greater killing of M. avium than did treatment of macrophages with TNF-alpha in the absence of anti-TGF-beta 1 antibody. In addition, macrophage monolayers treated with anti-TGF-beta 1 antibody before infection with M. avium showed mycobactericidal activity after stimulation with rIFN-gamma; in contrast, no effect of IFN-gamma was seen in monolayers not treated with anti-TGF-beta 1 antibody. We conclude that TGF-beta 1 produced after M. avium infection is a potent inhibitor of macrophage activation by cytokines. This inhibition may have an important role in the regulation of the immune response against M. avium.
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PMID:Production of transforming growth factor-beta by Mycobacterium avium-infected human macrophages is associated with unresponsiveness to IFN-gamma. 843 19

The induction of macrophage-deactivating (interleukin-10 [IL-10] and transforming growth factor beta [TGF-beta] and macrophage-activating (IL-1, IL-6, and tumor necrosis factor alpha [TNF-alpha] cytokines by lipoarabinomannan (LAM) from pathogenic Mycobacterium tuberculosis Erdman and H37Rv strains (ManLAM) and nonpathogenic mycobacteria (AraLAM) in human blood monocytes was examined. ManLAM was significantly less potent in induction of TNF-alpha, IL-1, IL-6, and IL-10 protein and mRNA, whereas its ability to induce TGF-beta was similar to that of AraLAM. Differences in induction of TNF-alpha mRNA by the two LAM preparations only became apparent at late time points of culture (24 h). The induction of TNF-alpha and IL-1 by purified protein derivative of M. tuberculosis was significantly stronger than that by ManLAM. Pretreatment of monocytes with ManLAM did not, however, interfere with cytokine induction by lipopolysaccharide or AraLAM. The extensive mannosyl capping of arabinose termini of ManLAM may underlie the lack of ability to induce some cytokines (IL-1, TNF-alpha, and IL-10) and the retained ability to induce TGF-beta. The latter may have a role in shifting the cytokine milieu in favor of survival of M. tuberculosis.
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PMID:Selective induction of transforming growth factor beta in human monocytes by lipoarabinomannan of Mycobacterium tuberculosis. 855 Jan 83

Previously we demonstrated that treatment of mice with either UVB radiation or supernatants derived from UVB-irradiated PAM 212 keratinocytes decreased the induction of the delayed-type hypersensitivity (DTH) response to Mycobacterium bovis bacillus Calmette-Guerin (BCG), impaired the clearance of bacteria from their lymphoid organs and also altered macrophage functions. In order to characterize the cytokines involved in these phenomena, UV-irradiated mice were injected with antibodies to interleukin-10 (IL-10), transforming growth factor-beta 1 (TGF-beta 1), or tumor necrosis factor-alpha (TNF-alpha). Injection of UVB-irradiated mice with anti-IL-10 immediately after UV irradiation restored the DTH response and reversed the UV-induced inhibition of bacterial clearance. Injection of UV-irradiated mice with anti-TGF-beta only partially restored the DTH response although it allowed a better clearance of BCG than injection of mice with the control antibody. In contrast, injection of anti-TNF-alpha did not affect the UVB-induced suppression of DTH or impaired bacterial clearance. Similarly, the ability of macrophages to phagocytose BCG and kill the intracellular organisms was restored to almost normal levels after injecting UV-irradiated mice with antibodies specific for IL-10 or TGF-beta. Injection of mice with either recombinant IL-10 or TGF-beta mimicked the effect of whole-body UV irradiation on immune function. These results suggest that IL-10 has a major role in UV-induced suppression of both DTH to BCG and impairment in the clearance of bacteria and that TGF-beta has a more significant role in blocking bacterial clearance. Furthermore, these cytokines seem to modulate immune responses by altering macrophage functions in UVB-irradiated mice.
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PMID:Mechanism of UVB-induced suppression of the immune response to Mycobacterium bovis bacillus Calmette-Guerin: role of cytokines on macrophage function. 876 May 65

Immunohistochemical studies were performed to determine the presence and distribution of polypeptide transforming growth factor (TGF)-beta 1, a cytokine with macrophage-suppressing activity, in skin biopsies from 41 patients with different clinical forms of leprosy. We used an anti-TGF-beta 1 polyclonal antibody and the avidinbiotin-peroxidase (ABC complex) method. The results demonstrated that the lesions of the lepromatous and borderline lepromatous forms presented intense cytoplasm staining for TGF-beta 1 in the cells of the dermal infiltrate. A reaction of moderate intensity was observed in the cells of granulomas from borderline borderline cases, whereas no detectable immunoreaction was observed in granuloma cells from the tuberculoid and borderline tuberculoid forms. Considering that in the lepromatous leprosy form Mycobacterium leprae multiplies in the cytoplasm of macrophages and the lesions are diffuse and consist of poorly differentiated young macrophages, we believe that these alternations may be explained at least in part by the presence of TGF-beta 1 in the dermal infiltrate. Production of the cytokine may be induced by the presence of the bacillus itself and of its constituents, causing a mechanism of parasite evasion. Similarly, the absence of TGF-beta 1 in tuberculoid leprosy, which progresses with a specific immune response to M. leprae, may explain the intense differentiation of macrophage cells with the formation of well defined epithelioid granulomas capable of eliminating most of the bacilli.
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PMID:Detection of transforming growth factor-beta 1 in dermal lesions of different clinical forms of leprosy. 877 45

We describe here a previously healthy, 42 year old, HIV-negative woman. Following a seemingly successful 2-year antimycobacterial regimen for a lung infection caused by Mycobacterium avium/intracellulare she acquired a lung infection caused by M. chelonei. Characterization of alveolar cells from bronchoalveolar lavage fluid using flow cytometry revealed a total lack of T-cell subset CD4+ helper lymphocytes in spite of a normal proportion of the CD3+ and CD4+ T-cells in peripheral blood. The levels of Th2 cytokines such as IL-4, TGF-beta and G-CSF were higher in the patient's alveolar cells than in the cells of 4 healthy controls. This imbalance of cells and cell cytokines may contribute to the patient's susceptibility for non-tuberculous mycobacteria and her failure to eradicate these microorganisms.
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PMID:Lack of T-helper lymphocytes in BAL fluid from a HIV-negative patient with recurrent non-tuberculous mycobacterial lung infections. 906 68

Coinfection with Mycobacterium tuberculosis and human immunodeficiency virus (HIV) is a serious problem, particularly in developing countries. Recently, M. tuberculosis and purified protein derivative (PPD) were demonstrated to induce HIV replication in CD8 T cell-depleted peripheral blood mononuclear cells from HIV-positive, PPD-positive persons but not in cells from PPD-negative persons. The role of endogenous and exogenous cytokines in modulating M. tuberculosis-induced HIV replication was evaluated. M. tuberculosis-induced HIV replication decreased following simultaneous inhibition of endogenous interleukin (IL)-2, IL-1beta, and tumor necrosis factor-alpha by the addition of soluble receptors and receptor antagonists or following exogenous IL-10 and transforming growth factor (TGF)-beta. In contrast, neutralization of endogenous IL-10 and TGF-beta augmented M. tuberculosis-induced HIV replication by increasing cellular activation. Thus, the balance between IL-2 and proinflammatory and antiinflammatory cytokines plays a major role in M. tuberculosis-induced replication of HIV.
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PMID:The in vitro induction of human immunodeficiency virus (HIV) replication in purified protein derivative-positive HIV-infected persons by recall antigen response to Mycobacterium tuberculosis is the result of a balance of the effects of endogenous interleukin-2 and proinflammatory and antiinflammatory cytokines. 959 21

Changes in Mycobacterium leprae-induced lymphoproliferative responses and mediator release by leprosy patients' lymphocytes were followed during multiple drug therapy (MDT). At the time of diagnosis, multibacillary (MB) patients who did not develop reactions responded to both sonicated M. leprae and synthetic disaccharide coupled to bovine serum albumin (ND-BSA) antigens, but those who would later develop reactions did not respond, even in the presence of added cytokines. The paucibacillary (PB) group initially had high responses to sonicated M. leprae but no response to ND-BSA, even in the presence of added cytokines. In the first year of treatment, the supernatants of PB patients' cell cultures contained factors that enhanced the phytohaemagglutinin (PHA) response of normal cells. In contrast, those MB patients who did not develop reactions at a later stage produced culture supernatants that were inhibitory. Interestingly, the MB patients who later developed reactions during treatment, and did not initially respond to M. leprae, produced supernatants containing enhancing factors, like those of the PB group. Later on in the treatment, all patients had the same patterns: when response to M. leprae decreased from its highest level, inhibitory factors were produced. Further studies revealed that the supernatants which inhibited the PHA response of normal cells contained the active form of transforming growth factor-beta 1, (TGF-beta 1), whatever the disease type or treatment status of the donor. These TGF-beta 1 levels correlated directly with the degree of inhibition. Similarly supernatants that neither inhibited nor enhanced PHA responses contained the highest levels of interleukin-10 (IL-10), while those from treated patients that enhanced contained the lowest levels of interleukin-4 (IL-4) and interferon-gamma (IFN-gamma). These cytokine correlations transcended the conventional disease classification, and imply that all patients pass through a sequence of patterns of immune response during treatment. These treatment-induced changes may explain occasional reports of response patterns at variance with the 'immunological spectrum' of leprosy.
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PMID:Changes in cellular response to mycobacterial antigens and cytokine production patterns in leprosy patients during multiple drug therapy. 974 41


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