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Biomedical subjects

M A Bach

Publications and source records attributed to M A Bach.

At least 145 records · Page 8Linked to original sources
PubMedDate not supplied

Phenolic glycolipid-1 from M. leprae inhibits oxygen free radical production by human mononuclear cells.

We studied the effect of PGL1, a phenolic glycolipid unique to Mycobacterium leprae, on the activation of the phagocyte oxidative respiratory burst, by measuring the chemiluminescence (CL) generated by normal mononuclear cells. PGL1 induced a decrease in oxygen free radical production stimulated by mycobacteria (M. leprae, BCG and M. kansasii) or by phorbol myristate acetate, but did not prevent the binding or ingestion of fluorescein-conjugated mycobacteria. In contrast, mycoside A from M. kansasii, a structurally related compound, did not alter the CL response. In addition, treatment of M. leprae with anti-PGL1 antibodies failed to restore the response to this microorganism. PGL1 could act as an oxygen species scavenger and protect M. leprae from killing by toxic oxygen metabolites.

Adult↗
PubMedDate not supplied

A monoclonal antibody against Mycobacterium lepraemurium which recognizes a cross-reacting mycobacterial antigen.

Spleen cells from BALB/c mice infected two weeks earlier with Mycobacterium lepraemurium were fused with myeloma cells, and, using an indirect immunofluorescence assay, a hybridoma was selected which secreted ananti-M. lepraemurium IgM antibody. In the same assay, this monoclonal antibody also recognized 17 other species of Mycobacteria (including M. leprae) and two strains of Nocardia.

Animals↗
PubMedDate not supplied

Mycobacterium leprae-reactive T-cell clones isolated from polar lepromatous and tuberculoid leprosy patients.

T-cell clones capable of mounting a proliferative response to Mycobacterium leprae were obtained in three leprosy patients (two polar lepromatous and one polar tuberculoid) either from M. leprae-activated or from protein-purified derivative-activated polyclonal T lymphoblasts. All these clones expressed the CD4 surface marker. Some of them proliferated to the antigen only in the presence of interleukin-2. A majority expressed cross-reactive responses to other mycobacteria. Clones obtained from the lepromatous patients did not differ in any of these features from those obtained from the tuberculoid patient. M. leprae-reactive clones obtained from one lepromatous patient displayed strong antigen-specific cytotoxicity toward autologous antigen-coated target cells. This phenomenon was not observed for any clone of the other lepromatous patient and was seen only for one clone in the tuberculoid patient.

Antigens, Bacterial↗
PubMedDate not supplied

Cyclic AMP and T-cell differentiation.

We have studied the effects of a circulating thymic factor (TF), cyclic AMP (cAMP) and prostaglandins on T-lymphocyte differentiation in the mouse using three parameters: 1) 0-bearing cell percentage evaluated by a cytotoxicity test with anti-0 serum (A0S) plus complement; 2) 0-antigen presence on rosette forming cells (RFC) assessed by the inhibition of rosette formation with A0S; 3) lymphocyte mediated cytotoxicity (LMC) against allogeneic target cells after in vivo sensitization, using a chromium release assay.

Animals↗
PubMedDate not supplied

T cell subsets in multiple sclerosis. A longitudinal study of exacerbating-remitting cases.

Twenty-four untreated MS patients with exacerbating-remitting disease were longitudinally studied for T-cell subset distribution within peripheral blood, using monoclonal antibodies OKT3, OKT4 and OKT8. A decreased percentage of OKT8 reactive cells, with a correlative increase of the OKT4/OKT8 ratio, was detected in relapsing MS patients, in most cases within 2 weeks before and 1 week after the onset of relapse. Longitudinal analysis of individual fluctuations allowed to detect during relapse an increase of OKT4/OKT8 ratio over the value recorded during remission in 78% of MS patients. Only 50% of patients however exhibited an OKT4/OKT8 ratio exceeding the 5% confidence upper limit of healthy control values. Relapse was more often associated with T-cell subset abnormalities in patients who suffered several attacks during the period of study. MS patients in remission, when considered as a group did not show significant abnormalities of the T-cell subset balance, although some individuals did present with wider T-cell subset fluctuations than healthy controls.

Adolescent↗
PubMedDate not supplied

Mechanisms of T-cell unresponsiveness in leprosy.

We analysed the mechanisms of T-cell unresponsiveness to Mycobacterium leprae antigens and to unrelated antigens or T-cell mitogens in human leprosy and in an experimental model of murine infection by M. lepraemurium (MLM). In human leprosy, monoclonal antibodies OKT3, OKT4 and OKT8 were used to enumerate T-cell subpopulations within peripheral blood. Increased percentages of OKT8+ cytotoxic/suppressor cells were observed in untreated, non-reactional lepromatous patients. Conversely, lepromatous patients suffering from erythema nodosum leprosum, an Arthus-like phenomenon, exhibited a transient drop in the percentage of OKT8+ cells with a correlative increase in the proliferative response to T-cell mitogens. We studied the proliferative response to M. leprae of OKT4+ and OKT8+ cells isolated by a negative selection procedure using antibody-induced cytotoxicity plus complement. None of these subpopulations proliferated when incubated with M. leprae. In some patients, control treatment of mononuclear cells with complement alone induced the reappearance of a strong proliferative response to M. leprae, suggesting the existence of an active suppressor mechanism through soluble factors of an unknown nature. In MLM-induced murine leprosy, a progressive decrease was observed in the proliferative response to concanavalin A (ConA), and an early decrease in interleukin 2 activity in supernatants from ConA-stimulated spleen cells. Splenic T cells from MLM-infected mice transferred into naive recipients accelerated the local MLM growth in these recipients, suggesting that suppressor T cells may play a pathogenic role in the progression of MLM infection.

Animals↗
PubMedDate not supplied

Antimycobacteria antibodies in M. lepraemurium murine infection.

Two groups of BALB/c mice were inoculated with either 10(7) or 10(5) MLM subcutaneously into the lefthind footpad. Mice receiving 10(7) MLM were followed throughout infection for granuloma size, and antibody production against sonicated M. lepraemurium (MLM), whole M. lepraemurium and whole M. triviale, using a radioimmunoassay. All mice were sacrificed at 37 weeks post infection and acid fast bacilli were enumerated in both footpads and in the spleen. Noticeable individual variations were observed in the pattern of progression of the granuloma, and in the resistance to the infection, as assessed by measurements of bacilli local growth and dissemination. Antibody formation against MLM sonicate was detected as early as at 6 weeks post inoculation, a time when granulomas started to develop. Antibody production increased further when the infection progressed, against MLM (sonicate or whole bacilli), as well as against whole M. triviale. No correlation could be found between antibody activity and local bacilli growth or bacilli dissemination. Mice receiving 10(5) MLM s.c. were followed for ganuloma size and antibody production against sonicated MLM or other sonicated mycobacteria (pool of 6 different species). Antibody production could be detected against MLM and other mycobacteria as soon as 4 and 8 weeks after infection respectively, i.e. several weeks prior to the appearance of granulomas, which occurred at 12 weeks of infection.

Animals↗
PubMedDate not supplied

Influence of dose and route of inoculation and of mouse strain on the production of interleukin 2 in mice infected with Mycobacterium lepraemurium.

In order to evaluate the influence of route and dose of inoculation on interleukin 2 (IL2) production, C57BL/6 mice were infected either intravenously (I.V.) or subcutaneously (S.C.) with 10(5) or 10(8) Mycobacterium lepraemurium. The role of genetic factors on the production of IL2 during M. lepraemurium infection, was investigated in 7 inbred mouse strains (C57BL/6, DBA/2, F1 (C57BL/6 X DBA/2), DBA/1, BALB/c, CBA and A/J) after I.V. infection with 10(7) M. lepraemurium. At different times after M. lepraemurium inoculation, the number of AFB within the spleens of infected mice was counted and the ability of Con A-activated spleen cells to produce IL2 was studied. In S.C. inoculated C57BL/6 mice the increase in footpad thickness was measured during the progression of infection. After one month of infection heavily infected C57BL/6 mice (10(8) bacilli) showed an early and strong deficiency of IL2 production, regardless of the route of inoculation, whereas mice infected with a lower dose (10(5) bacilli) did not. In S.C. infected mice the decrease of IL2 production was observed when the footpad enlargement reached to the plateau phase. The data obtained from the numeration of AFB within the spleens of infected mice allowed to rank the infected mouse strains into 2 separated groups according to the pattern of the Bcg gene expression. An IL2 deficiency was only observed in C57BL/6, DBA/1, (C57BL/6 X DBA/2)F1 and DBA/2 infected mouse strains. No evident correlation could be shown between splenic IL2 activity upon Con A stimulation and the number of AFB recovered from the spleens of these 7 inbred mouse strains.

Animals↗