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)

Acetone-killed Mycobacterium leprae separated from infected armadillo liver tissue without the use of proteases were treated with 0.2 M lithium acetate, 20 mM EDTA, pH 8.8 solution, and the concentrated antigen extract was analyzed by Ouchterlony immunodiffusion. The antigen extract gave a single immunoprecipitate when reacted with pooled lepromatous leprosy (LL) patients sera made highly specific for M. leprae by adsorption. Apparently identical precipitates were produced by reacting the antigen extract with sera of each of 15 treated LL patients, 5 of 7 patients with tuberculoid leprosy, and 3 of 4 M. leprae infected armadillos. Serum from 1 of 16 persons immunized with BCG and from none of 15 patients with chlamydial urethritis or brucellosis reacted with the antigen. Identically prepared extracts of M. smegmatis, M. phlei, M. vaccae, M. duvali and M. diernhoferi gave no immunoprecipitates with sera from LL patients or infected armadillos. Preliminary characterization indicates the antigen is protein since antigenicity was destroyed by pronase and/or heat treatment. The relative specificity of the protein antigen for M. leprae and the presence of antibody to this antigen in patients with leprosy suggest a possible role for this antigen in the serodiagnosis of leprosy.
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PMID:Identification of a Mycobacterium leprae specific protein antigen(s) and its possible application for the serodiagnosis of leprosy. 9 Jun 66

Five patients with active leprosy, four with polar lepromatous (LL) and one with borderline lepromatous (BL) disease, were each treated with transfer factor (TF) from approximately 7.4 x 10(9) lymphocytes given in 36 divided doses over a 12-week period. The TF was prepared from blood donated by normal, healthy, lepromin skin test-positive individuals. During treatment all four of the LL patients, but not the BL patient, developed clinical reversal reactions. Histopathologically, skin biopsies in these four LL patients showed evidence of transformation of collections of multibacillary macrophages into paucibacillary epithelioid cells and giant cells. To our knowledge, this is the first histopahtologic documentation of reversal reactions occurring in polar LL. To the extent that reversal reactions are evidence of effective cell-mediated immunity of Mycobacterium leprae, these results indicate that TF is capable of at least partial correction of the immunologic deficit of lepromatous leprosy.
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PMID:Reversal reactions in lepromatous leprosy following transfer factor therapy. 71 42

Patients with borderline-lepromatous (BL) or fully lepromatous (LL) leprosy were treated in the sanitarium for approximately 1 year with oral rifampin (600 mg daily) or with oral dapsone (100 mg daily). They were then treated as outpatients with intramuscular acedapsone (225 mg every 12 weeks) or oral dapsone (50 mg daily). They have now been followed for a total of 28 to 34 months. Death of Mycobacterium leprae during the initial 24 weeks was monitored by mouse inoculation with M. leprae from skin punch biopsy specimens. With rifampin therapy, death of M.leprae occurred rapidly, and viable M. leprae were nearly undetectable by the time the first specimen was taken after the start of treatment, at 4 weeks. With dapsone therapy, death of M. leprae was slower, and in some cases the inoculation results were still positive at 12 weeks. The therapeutic response during the period of outpatient treatment has been satisfactory. The number of dead M. leprae, as measured by the bacterial index in skin smears and the number of acid-fast bacteria in skin specimens, has continued to decrease, and clinical progress has been satisfactory. The measured drug-induced death of M. leprae occurred at about the same rate in BL patients as in LL patients. Disappearance of dead M. leprae from the tissues was much more rapid in BL patients than in LL patients.
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PMID:Rifampin therapy of lepromatous leprosy. 109 95

The effect of circulating immune complexes, isolated in the form of polyethylene glycol (PEG) precipitates from leprosy patients, on lymphocyte proliferation was studied. The results obtained showed that PEG precipitates obtained from the borderline lepromatous/lepromatous (BL/LL) types of leprosy patients and those undergoing erythema nodosum leprosum (ENL) had significant suppressive effects on the lymphocyte proliferation induced by Mycobacterium leprae antigens in healthy responders. The percent decreases in the mean values of delta cpm in the presence of PEG precipitates from the BL/LL and ENL groups were found to be 46.8 +/- 22.4 and 65.0 +/- 24.3, respectively. However, no significant suppressive effects (except for ENL PEG precipitates) of these PEG precipitates were observed on the lymphocyte proliferation induced by tuberculin (PPD). Further, PEG precipitates alone (in the absence of M. leprae antigen) from the BL/LL and ENL groups were found to have no effect on the lymphocyte proliferation.
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PMID:Suppressive effect of circulating immune complexes from leprosy patients on the lymphocyte proliferation induced by M. leprae antigens in healthy responders. 129 11

1. Studies were carried out to determine the effect of intra-dermal injections of recombinant human interferon-gamma (rIFN gamma) on the viability of Mycobacterium leprae. Twenty-three untreated and 4 treated multibacillary patients, 12 with lepromatous leprosy (LL) and 15 with borderline lepromatous leprosy (BL), were selected for intradermal administration of rIFN gamma or PPD. Treated patients (LL and BL) had received multi-drug therapy according to the recommendations of the World Health Organization, i.e., rifampicin (600 mg/month), dapsone (100 mg/day) and clofazimine (50 mg/day and 300 mg/month) for 1-4 months. Three daily doses of 10 or 30 micrograms rIFN gamma induced local induration and mononuclear leucocyte accumulation. Bacteria isolated from a punch biopsy of the site 21 days after lymphokine administration were injected into mouse foot pads and evaluated for viability and growth. 2. The local response to rIFN gamma (specific activity 2 x 10(7) units/mg protein) induced a delay or total inhibition of M. leprae growth in the mouse foot pad, indicating that the cellular response to the antigen reduced local M. leprae viability. The extent of reduction in viability depended on the dose of rIFN gamma injected and the extent of local induration induced by the lymphokine. With a vigorous cell-mediated immune response growth was fully inhibited. 3. A similar but less extensive effect on M. leprae viability was observed in response to the local injection of 5 units in 0.1 ml of purified protein derivative of tuberculin (PPD).
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PMID:Effect of cutaneous cell-mediated immune response to rIFN gamma on Mycobacterium leprae viability in the lesions of lepromatous leprosy. 134 21

Because of the good results obtained in the mononuclear cell (T lymphocyte) proliferative response in tuberculoid leprosy patients and family contacts and healthy Mitsuda-positive volunteers using Mycobacterium leprae soluble extract, we prepared different protein fractions from the soluble extract. We used the T-cell Western blot technique with separation by electrophoresis in SDS-polyacrylamide gels and transfer onto nitrocellulose membranes. Each unstained blot was converted into 18 fractions of antigen-bearing particles and tested with peripheral blood mononuclear cells from 21 individuals including Mitsuda-positive contacts, vaccinated lepromatous leprosy (LL) patients, borderline tuberculoid (BT) patients, and unvaccinated lepromatous patients. The stimulation index (SI) of the contacts was higher to the different fractions in comparison with the leprosy patients. They showed four peaks of stimulation to fractions 66-55, 45-29, 22-18, and 14 kDa. The second highest responders were BT patients, followed by vaccinated LL patients. The unvaccinated patients did not respond significantly to any of the fractions (SI less than 1).
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PMID:Preliminary study of cellular immunity to Mycobacterium leprae protein in contacts and leprosy patients. 152 61

Sera from 173 leprosy patients with various types of disease (tuberculoid = TT, borderline tuberculoid = BT, borderline lepromatous = BL, and lepromatous = LL), 12 intrafamilial contacts, and 40 normal healthy individuals were assayed in an indirect enzyme-linked immunosorbent assay (ELISA) using Mycobacterium leprae antigens. Recombinant clones carrying M. leprae antigens, namely, Y3184 (12 kDa), Y3179 (18 kDa), Y3164 (28 kDa), Y3180 (36 kDa), and Y3178 (65 kDa) and a cell sonicate from armadillo-derived M. leprae were used for the study. A high degree of reactivity with the 65-kDa, 36-kDa, and 28-kDa protein lysates was observed in most of the sera from multibacillary patients, with a low degree of positivity with 18 kDa and 12 kDa. Only a few sera from paucibacillary patients showed positive reactions. The majority of the contacts' sera tested showed no reactivity with these antigens.
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PMID:Sero-immunoreactivity of cloned protein antigens of Mycobacterium leprae. 152 62

A total of 90 leprosy patients, 12 household contacts and 10 normal subjects were studied for the detection of Mycobacterium leprae cell wall antigen in urine using monoclonal antibody (ML30A2 IgG). In untreated multibacillary leprosy (BL-LL) the M. leprae cell wall antigen could be demonstrated in the urine of 14 (64%) patients by immunofluorescence (IF) and 22 (100%) by ELISA. In untreated paucibacillary leprosy (TT-BT), it could be demonstrated in 3 (11.5%) and in 13 (50%) patients by IF and ELISA methods respectively. All but 1 household contact (later confirmed to have BL leprosy) and all 10 normal subjects' urine was negative for M. leprae cell wall antigen by both methods. The same antigen was, however, demonstrated in urine of 50% paucibacillary patients who had received 6 months of treatment and in 68% multibacillary patients who had received 24 months of WHO recommended multidrug therapy. M. leprae cell wall antigen assays in urine will not be useful in the follow-up of leprosy patients on multidrug therapy.
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PMID:Detection of a Mycobacterium leprae cell wall antigen in the urine of untreated and treated patients. 156 13

Sonicated extracts of Mycobacterium leprae were separated by two-dimensional gel electrophoresis and electroeluted into 400 distinct soluble fractions. These fractions were probed with T lymphocytes from leprosy patients of different disease types, healthy contacts, and unexposed healthy individuals. Proliferative responses were visualized using three-dimensional stimulation profiles. T cells from many patients and contacts responded to a multitude of antigen fractions of different molecular masses and isoelectric points. T cells from unexposed individuals gave significant responses to lysates or whole organisms of M. leprae, but no or only marginal responses to separated antigen fractions. T cells of polar tuberculoid (TT) and the majority of polar lepromatous (LL) leprosy patients responded only to separated antigen fractions but not to lysates or whole organisms of M. leprae. The remaining LL patients were totally unresponsive and even failed to respond to separated M. leprae fractions. Thus, in some leprosy patients unresponsiveness to M. leprae seems to be caused by distinct components and can be broken by using separated antigen fractions; whereas in others, anergy remains. T cells of borderline tuberculoid (BT) patients, who were under chemotherapy, responded to separated antigen fractions as well as to lysates of M. leprae organisms. In contrast, BT patients who were untreated failed to react with any of the M. leprae preparations. Similarly, T cells of the majority of LL patients responding to separated fractions were under chemotherapy; whereas T cells from untreated LL patients gave no or only marginal responses to any of the M. leprae antigen preparations. These findings suggest some linkage between the degree of T-cell responsiveness and antileprosy drug treatment.
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PMID:T-cell responses of leprosy patients and healthy contacts toward separated protein antigens of Mycobacterium leprae. 160 93

Antigenic determinants of Mycobacterium leprae were identified by screening a lambda gt11::M. leprae genomic library with two separate pools of sera from leprosy patients. A total of 45 recombinant clones were detected with pooled sera from 21 lepromatous (LL) leprosy patients and 5 additional clones specified polypeptides that reacted with antibodies in pooled sera from 30 borderline tuberculoid or tuberculoid leprosy patients. The recombinant clones that specified antigenic determinants that reacted with sera from LL patients were condensed into eight groups on the basis of DNA hybridization experiments among the M. leprae DNA insert fragments. In addition, 11 of the 45 recombinant clones did not hybridize to members of the eight groups nor to one another; these represent unique recombinant clones. None of the recombinant clones identified by screening with sera from tuberculoid leprosy patients hybridized to each other or to any of the 45 LL recombinant clones. The polypeptides specified by the recombinant clones were usually fusion proteins with beta-galactosidase, ranging in size from 117 to 175 kilodaltons (kDa). Members of hybridization group III specified nonfusion proteins of 45 kDa. Only members of hybridization group I reacted with any of 30 monoclonal antibodies prepared against M. leprae proteins; recombinant proteins from these clones reacted with a single monoclonal antibody directed against the M. leprae 65-kDa protein. Thus, at least 22 new antigenic determinants of M. leprae have been identified on the basis of their reactivity to antibodies in sera from LL patients or sera from tuberculoid leprosy patients or both.
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PMID:Identification and characterization of antigenic determinants of Mycobacterium leprae that react with antibodies in sera of leprosy patients. 169 Nov 43


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