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P Launois

Publications and source records attributed to P Launois.

At least 73 records · Page 4Linked to original sources
PubMed1992

Anti-peripheral nerve antibodies in leprosy patients recognize an epitope shared by the M. leprae 65 kDa heat shock protein.

Binding of leprosy sera to peripheral nerve from different species (mouse, guinea pig and rabbit) was evaluated by ELISA. A majority of sera, whatever the clinical form of leprosy, bind to these antigens. Absorption with Mycobacterium bovis BCG demonstrated that these antibodies recognize cross-reactive epitopes between peripheral nerve and mycobacteria. In immunoblot analysis, both leprosy patient sera and a monoclonal antibody directed at the 65 kDa heat shock protein of M. leprae were shown to react with a heat-shock 67-68 kDa sciatic nerve protein. Binding of the monoclonal antibody to this sciatic nerve antigen was prevented by incubation with lepromatous patient sera, showing that some peripheral nerve epitopes recognized by patient antibodies are shared by the 65 kDa heat shock protein of M. leprae.

Animals↗
PubMed1992

TNF-alpha failed to reverse the M. leprae-induced defective chemiluminescence response of human mononuclear cells.

The effect of phagocyte activation by TNF-alpha on the ability to trigger a chemiluminescence (CL) response, associated with the release of oxidizing species was evaluated in healthy human mononuclear cells in the presence of Mycobacterium leprae. Recombinant TNF-alpha (r-TNF-alpha) increased the CL response of unstimulated M. bovis BCG- and PMA-stimulated cells but did not reverse the M. leprae defective activation of the human phagocyte oxidative burst. M. leprae was less well phagocytosed than M. bovis BCG but phagocytosis of mycobacteria was not altered by addition of r-TNF-alpha. The failure of activation of oxygen-free radical production might have some relevance to the pathogenesis of leprosy.

Humans↗
PubMed1992

Humoral responses against the 85A and 85B antigens of Mycobacterium bovis BCG in patients with leprosy and tuberculosis.

Immunoglobulin G antibodies against the 85A and 85B components of the Mycobacterium bovis BCG antigen 85 complex separated by isoelectric focusing were investigated in serum samples from 129 patients representing the major forms of leprosy, 111 tuberculous patients, and 153 healthy subjects. For both of the antigens, a higher degree of staining was observed for lepromatous leprosy patients and patients with active tuberculosis than for the other groups. Because sera from some healthy subjects recognized the 85A antigen, we suggest that antigen 85B is the most useful component of the antigen 85 complex for the serodiagnosis of the multibacillary forms of leprosy or of the active forms of tuberculosis.

Antibodies, Bacterial↗
PubMed1992

[Diagnosis of tuberculosis by specific DNA amplification directly in samples].

The polymerase chain reaction (PCR was used to identify M. tuberculosis in specimens from patients with suspected pulmonary tuberculosis. A segment of the IS 6110 sequence and of the Cro EL gene were amplified and identified by hybridization with specific probes labeled with peroxidase. The results are in agreement with those obtained using standard microbiological techniques or clinical criteria. The PCR method allowed the detection of M. tuberculosis in 22 out of 58 samples that were acid fast staining negative. The number of patients with at least one positive sample by PCR was much higher in the group with suspicion of tuberculosis (14/28) than in the control group (3/23). This demonstrates the possibility of using PCR technology in endemic areas for tuberculosis.

DNA, Bacterial↗
PubMed1992

[Epidemiological study of HIV seroprevalence in a leprosy patient population in Senegal].

We report the findings of an epidemiological study conducted between June 1989 and February 1990 on a population of leprosy patients in southern Senegal (Bignona major endemic disease sector). Two types of population were studied: patients living in urban areas and inmates of leprosaria. The global HIV seroprevalence (HIV 2 in all cases) of the leprosy-patient population was 1.15% (3/257): 0.8% (1/130) for the urban group and 1.5% (2/127) for the leprosaria. The seroprevalence rate does not differ significantly from that for the control group studied and for blood donors (1/221). The diagnosis of leprosy in the seropositive subjects had been established before 1980. None of them showed any sign of relapse. The immunodepression associated with the presence of HIV was only moderate: it was reflected in a lowering of the CD4 count and of the CD4/CD8 ratio, but with no clinical sign of AIDS.

Adolescent↗
PubMed1992

Human phagocyte respiratory burst by Mycobacterium bovis BCG and M. leprae: functional activation by BCG is mediated by complement and its receptors on monocytes.

We have measured the role of serum components on two parameters of the phagocytosis reaction: a) the chemiluminescence (CL) response associated with the oxidative respiratory burst in response to Mycobacterium bovis BCG and M. leprae, and b) the uptake of these two mycobacteria by healthy human monocytes. Pre-incubations of fresh or heat-inactivated serum or serum containing EGTA or EDTA indicate that these two mycobacteria activate the alternative complement pathway. Monoclonal antibodies against CR1 and CR3 inhibit the responses of M. bovis BCG and M. leprae, demonstrating that complement receptors mediate the phagocytosis of these two mycobacteria. Thus, complement and its receptors on the surface of the monocytes (CR1 and CR3) are important in the functional activation of phagocytosis of M. bovis BCG and M. leprae.

Antibodies, Monoclonal↗
PubMed1992

[Cytokines and leprosy].

One of the functions expressed by the effectors of the immune system is the synthesis of cytokines, either in soluble form or associated with the membrane. Study of this communication network between the different compartments of the immune system can be conducted either in the blood (serum) of leprosy patients or directly in the infected tissues. The key to how the immune response will develop lies in the nature of the cytokines produced locally by the immune cells. For the characterization and detection of cytokines/lymphokines we may use either biological methods (bioassay), or antibody-based detection systems (RIA, Elisa, Elispot, immunocytochemistry using monoclonal antibodies), or techniques derived from molecular biology (Polymerase chain reaction-PCR, analysis of messenger RNA, and hybridization in situ). These various techniques, whose advantages and disadvantages are discussed, have demonstrated that locally, in the infected lesions, resistance and/or susceptibility to M. leprae infection correlates with differing cytokine secretion profiles.

Biological Assay↗
PubMed1991

An isoelectric focusing method for the study of the humoral response against the antigen 85 complex of Mycobacterium bovis BCG in the different forms of leprosy.

Isoelectric focusing was used to separate the three components of the antigen 85 complex of Mycobacterium bovis BCG. Antibody responses of leprosy patients against each Mycobacterium bovis BCG. Antibody responses of leprosy patients against each component were quantitated by densitometric analysis of immunoblot assays. The 85A component was recognized by 40% (8/20) of the lepromin positive and negative healthy subjects, by 76% (19/25) of the tuberculoid and by 96% (24/25) of the lepromatous leprosy sera. In contrast, the 85B component was not stained by the control sera, nor by the tuberculoid leprosy sera but by 64% (16/25) of the lepromatous leprosy sera. The results suggest that antigen 85B contains one or several epitopes that are specifically recognized by sera of lepromatous leprosy patients only.

Antibodies, Bacterial↗
PubMed1991

T cell response to purified filtrate antigen 85 from Mycobacterium bovis Bacilli Calmette-Guérin (BCG) in leprosy patients.

T cell proliferation and IFN-gamma production of peripheral blood mononuclear cells from 25 healthy controls and 39 leprosy patients were tested against BCG-bacilli and culture filtrate. Mycobacterium leprae and purified antigen 85 (the major secreted 30-32 kD protein antigen) from M. bovis strain BCG. In lepromin negative healthy controls, blastogenesis was low to M. leprae and completely negative to antigen 85. IFN-gamma levels were very low, close to detection limits. In all lepromin positive controls, significant proliferation and IFN-gamma secretion was found in response to M. leprae and antigen 85. In the group of lepromatous leprosy (LL) patients, 25/29 of patients (with either positive (13) or negative (12) lymphoproliferative response to BCG) were unreactive to M. leprae or to antigen 85. Four LL patients with positive T cell response to BCG responded with detectable lymphoproliferative response and IFN-gamma secretion to antigen 85. All tuberculoid (TT) leprosy patients responded to BCG, M. leprae and antigen 85. Hence, T cells from leprosy patients and controls demonstrate a marked parallelism of responsiveness towards whole M. leprae and purified antigen 85 from M. bovis BCG, suggesting strong cross-reactivity between the two species and underlining the biological importance of such secreted antigens.

Antigens, Bacterial↗
PubMed1991

M. leprae- and BCG-induced chemiluminescence response of monocytes from leprosy patients and healthy subjects: effects of gamma-interferon and GM-CSF.

Mycobacterium leprae, in contrast to BCG, failed to trigger any chemiluminescence (CL) response in mononuclear cells from either leprosy patients or healthy subjects, a deficit not reversed by either interferon-gamma or GM-CSF. Chemiluminescence responses induced without mycobacteria or with BCG were found to be lower in leprosy patients than in controls. M. leprae were also less well phagocytosed than BCG. However, there was a significant difference in phagocytosis between healthy and tuberculoid leprosy subjects. Phagocytosis was not altered by the addition of either lymphokine, and no major differences between healthy subjects and patients were observed. Preincubating mononuclear cells with anti-mycobacteria antibodies (lepromatous patients' sera) did not increase the CL response nor the phagocytosis of M. leprae or BCG.

Antibodies, Bacterial↗
PubMed1990

[Research on malaria vaccine].

Malaria is an important public health problem in developing countries. The production of a good vaccine needs a better knowledge of different mechanisms which control the immune system. Results from donors show a higher frequency of antigens HLA: A2, B35, CW4, CW6, DRW52, DQW1 and DQW3. The lymphoproliferation in vitro of mononuclear cells, T cells and CD4+ and CD8+ subsets T cells with merozoite extracts is not so clear to establish a correlation between HLA phenotypes and T cells response.

Adult↗
PubMed1989

Human phagocyte oxidative burst activation by BCG, M. leprae, and atypical mycobacteria: defective activation by M. leprae is not reversed by interferon gamma.

The activation of the phagocyte oxidative respiratory burst by various mycobacteria was evaluated in an in vitro assay, by measuring the chemiluminescence, associated to the release of oxidizing species, generated by normal human whole blood phagocytes. All mycobacterium species, except Mycobacterium leprae, induced a significant chemiluminescence response. The strongest stimulus was provided by BCG, followed by M. triviale, M. chelonei, and M. fortuitum. M. kansasii, M. intracellulare, and M. lepraemurium elicited a weak response, although higher than that triggered by M. leprae. Both polymorphonuclear and mononuclear cells contributed to the whole blood cell chemiluminescence stimulated by mycobacteria, mononuclear cells being more efficient on a per cell basis. Phagocyte activation by recombinant interferon gamma did not improve M. leprae ability to trigger a significant chemiluminescence response. The failure of M. leprae and of some atypical mycobacteria to stimulate a strong phagocyte oxidative respiratory burst may have some relevance to their pathogenicity.

Adult↗
PubMed1989

Follow up of T cells subsets and anti-trisaccharide IgM antibody levels of leprosy patients during daily multidrug therapy.

T cell subset distribution and anti-M. leprae specific antibody levels were followed in leprosy patients during polychemotherapy (or multidrug therapy, MDT). Before treatment, the T cell subset counts showed that the multibacillary patients (28) have a significant decrease (p less than 0.05) in the CD3+, CD4+ T percentages and CD4+/CD8+ ratio as compared to the healthy controls (96). The paucibacillary patients (30) had no significant T cell disturbances. An ELISA test has been developed using the natural trisaccharide-ocytl-BSA (NTO) antigen to identify specific IgM antibodies (IgM anti-T). Multibacillary patients (22) showed higher antibody titers than paucibacillary patients (11). But the IgM anti-T levels of the two groups are significantly higher than controls belonging to the same ethnic group. A daily polychemotherapy (Dapsone, Rifampicine, Clofazimine) was done for 6 months in paucibacillary patients and 2 years in multibacillary patients according to the leprosy group study recommendations (Prof. Grosset, Hôptical de la Salpêtrière, Paris, France). A normalization of the CD4+ T cells was obtained by a 6 month therapy in multibacillary patients and a significant decrease in the IgM anti-levels was obtained during polychemotherapy in multibacillaries (p less than 0.001) and paucibacillaries (p less than 0.05).

Antibodies, Bacterial↗
PubMed1989

[Macrophage activation and Mycobacterium leprae: effect of interferon gamma on the production of oxygen free radicals by phagocytic cells].

Activation of the respiratory metabolic channel (F.O.R.), responsible in part for the bactericidal effect, was measured in vitro by a chemoluminescence test on circulating phagocytes. All mycobacteria tested, except for Mycobacterium leprae, induced a significant response. Its effect on lepromatous leprosy pathology is a subject for discussion.

Free Radicals↗
PubMed1988

Mechanisms of Mycobacterium leprae-specific T-cell deficiency in lepromatous leprosy.

Patients suffering from lepromatous leprosy fail to develop an efficient cell-mediated immunity towards Mycobacterium leprae, the causative agent. The mechanism of such a specific T-cell tolerance to the bacillus remains a key question in the pathophysiology of leprosy. Macrophages do not show any intrinsic defect in phagocytizing and killing M. leprae or in presenting antigen to helper T-cells. On the other hand, M. leprae-reactive helper T-cells do persist in lepromatous patients, but their activation appears to prevented by active suppressor mechanisms, involving both suppressor T-cells and macrophages. The target of this specific suppression could be the interleukin 2-producing T-cell subset. A better molecular definition of M. leprae antigens, both by monoclonal antibodies and T-cell clones, should open new perspectives for further analysis of the regulation of immune responses to M. leprae.

Immune Tolerance↗