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Biomedical subjects

L Dubertret

Publications and source records attributed to L Dubertret.

At least 217 records · Page 12Linked to original sources
PubMed1991

[Clinical aspects commented on].

Psoriasis is a chronic and common disease (prevalence of 1/1000 in France). It is therefore highly probable that it will be encountered by all non-dermatologists in their practice, hence the necessity for them to be able to recognize its principal forms. The clinical presentations of psoriasis are multiple and varying in their severity. In any given patient flare-ups may constantly be similar or change in the course of time. In the vast majority of cases skin lesions are typical, leading to a purely clinical diagnosis without need for additional investigations, and treatment can be instituted. In some case, however, the lesions are atypical and the diagnosis is doubtful. This is where histological skin biopsy can be of considerable help. Finally, other skin lesions may resemble psoriasis and be misleading; here again, histology or some other laboratory examinations will provide the correct diagnosis. In this chapter all these situations are presented be means of photographs accompanied with comments, which illustrate the semeiological and clinical diversity of psoriasis.

Humans↗
PubMed1991

[Psoriasis. Therapeutic strategy].

The strategy of psoriasis treatment consists first in informing the patients about the too quick renewal of their skin with, as a consequence, the necessity of two phases in the treatment; the clearing phase aimed at suppressing the skin lesions, and a maintenance phase where it is necessary to continue the treatment on an apparently normal skin in order to avoid relapse. For local treatments (tar, anthralin, topical local steroids, mechlorethamine, vitamin D3 derivatives and ointment) and for systemic treatment (UVB, PUVA therapy, retinoids, cyclosporine or methotrexate) it is necessary that the inconvenience of the treatments (due to modifications in everyday life and due to side effects) be less important than the decrease of life quality due to psoriasis. The aim is not to clear psoriasis but to increase the quality of life of the patients. A peculiar strategy of treatment is necessary for some forms of psoriasis like flexural psoriasis, psoriasis arthritis, ungueal psoriasis, palmoplantar psoriasis, pustular psoriasis, psoriatic erythroderma and psoriasis of the child. With the various treatments that we have now, used alone or in association, it is possible to improve the quality of life of nearly all psoriatic patients.

Administration, Cutaneous↗
PubMed1991

UVA-induced lipid peroxidation in cultured human fibroblasts.

The UVA irradiation of cultured human fibroblasts leads to the formation and to the release of thiobarbituric acid-reactive substances in the supernatant. The major thiobarbituric acid-reactive substance is identified by fluorescence spectroscopy and HPLC, as malondialdehyde or malondialdehyde-forming substances under the thiobarbituric acid assay conditions. Malondialdehyde formation strongly suggests a UVA-induced lipid peroxidation. Lipid peroxidation is also supported by the inhibitory effect of D,L-alpha-tocopherol, the well-known chain breaking antioxidant, by the additional malondialdehyde formation in the dark after the photooxidative stress and by membrane damage revealed by lactate dehydrogenase leakage.

Cell Membrane↗
PubMed1991

Paf-acether in human skin.

Paf is a phospholipid mediator present in human skin which induces inflammatory events, such as neutrophil infiltration and increased vascular permeability. Recent data suggest that cutaneous cells, such as fibroblasts and keratinocytes, produce paf and that paf is released during allergic cutaneous reactions. It is tempting to speculate that paf may contribute to the development of various skin disorders with acute and chronic skin inflammation. Paf antagonists may help in bringing answers to this hypothesis and may offer new prospects for the treatment of cutaneous inflammatory diseases.

Humans↗
PubMed1991

Cyclosporin A inhibits the antigen-presenting functions of freshly isolated human Langerhans cells in vitro.

Cyclosporin A (CsA) is a strong inhibitor of skin allograft rejection. It has been also reported to act, not only on helper T cells, but also on the antigen-presenting functions of mouse epidermal cells (EC) enriched in Langerhans cells (LC). We tested the effects of CsA on the human allogeneic mixed epidermal cell-lymphocyte reaction (MECLR) using whole EC and freshly isolated LC as stimulator cells. Results were as follows. 1) CsA inhibited the lymphocyte proliferative response in a dose-dependent fashion, by about 80% for a CsA concentration of 10(-7) M. To evaluate the effects of the drug on the two cell populations involved in MECLR, stimulator EC and responder PBMC were separately pulsed for 2 h with CsA, washed, and combined to form MECLR. Inhibition by CsA of the alloantigen-dependent lymphocyte proliferation appeared to be multifactorial, because CsA-pulsed EC and CsA-pulsed effector PBMC led to identical reductions of 40% each in proliferation. 2) The nature of EC sensitivity to CsA during MECLR was then analyzed after freshly separating highly purified CD1-positive LC (greater than 95%) and LC-depleted EC (mainly keratinocytes), using an immunomagnetic particle technique. When responder PBMC were cultured with CsA-pulsed LC, a highly significant reduction of lymphocyte proliferation was observed, indicating that CsA has direct effects on LC. 3) Some of the possible mechanisms by which CsA might act on LC were studied. Substantial IL-1 activity and PGE2 amounts were induced during MECLR by LC and keratinocytes, but CsA did not act via these factors. Neither did it significantly modify HLA-DR, DQ, or DP antigen expressions on EC. In conclusion, CsA directly inhibits antigen presentation by human LC. This inhibition may partly explain the beneficial effects of CsA on skin allografts and certain cutaneous immune reactions.

Adolescent↗
PubMed1991

Cicatricial pemphigoid antigen differs from bullous pemphigoid antigen by its exclusive extracellular localization: a study by indirect immunoelectronmicroscopy.

Several components of the dermal-epidermal junction (DEJ) bear the name of the autoimmune bullous disease in which they are involved. The epidermolysis bullosa acquisita (EBA) antigen, a component of anchoring fibrils, and the bullous pemphigoid (BP) antigen, a component of hemidesmosomes (HD) with a molecular weight of 220-240 kD, have been well characterized. In contrast, there is little data known about the cicatricial pemphigoid (CP) antigen. No differences between CP and BP have been reported when sera of patients were studied by Western immunoblotting. Findings of a study of sera from 8 patients with CP by indirect immunoelectron microscopy (IEM) on normal human skin are reported. Saponin (0.1% 10 mn) was used as a permeabilizing agent of cytomembranes and saponin-treated skin samples were compared to saponin-untreated skin samples. Four sera from patients with BP, one from a patient with EBA, and three from healthy donors served as controls. The CP sera produced a similar staining of DEJ on both saponin-treated and saponin-untreated skin samples: immune deposits were localized over the lamina densa and the lower part of the lamina lucida clearly separated from the cytoplasmic membrane of keratinocytes, in regularly spaced clumps. The BP sera produced an intense staining of DEJ only on saponin-treated skin samples: immune deposits were observed on the cytoplasmic attachment plaque of the HD; on saponin-untreated skin samples, BP sera produced only a faint staining of the extracellular part of HD. Finally, as expected the EBA serum appeared on the lower part of the lamina densa and anchoring fibrils, and no DAB deposits were observed with the serum of healthy donors. This data indicated that CP antigen is different than BP antigen by its exclusive extracellular localization. It may be a component of anchoring filaments.

Autoantigens↗
PubMed1991

Growth stimulation of human keratinocytes by tissue inhibitor of metalloproteinases.

Human recombinant tissue inhibitor of metalloproteinases (rTIMP) at 0.2-4.6 microM was found to stimulate the growth of normal human keratinocytes, in primary cultures on a plastic support, and to markedly increase their growth on a tridimensional culture system, the skin equivalent, as shown by histology, DNA measurements, and planimetry. In contrast, rTIMP had no effect on the growth of normal human fibroblasts. The growth of keratinocytes on extracellular matrix components produced by keratinocytes cultured in the presence or absence of rTIMP was similar, suggesting that rTIMP does not stimulate keratinocyte growth by modifying either the quantity or the composition of the extracellular matrix deposited. rTIMP was labeled with 125iodine in order to study its interaction with keratinocytes in culture. Binding of (125I) rTIMP to keratinocytes was found to be temperature and time dependent. Under steady-state conditions at 22 degrees C, one class of specific rTIMP binding sites was identified with KD of 8.7 nM and 135,000 sites/cell. Such findings are in keeping with the known potentiating effect of TIMP on erythroid precursors, and indicate that this protein has at least two distinct activities.

Binding Sites↗
PubMed1991

Activities of human acidic fibroblast growth factor in an in vitro dermal equivalent model.

Acidic fibroblast growth factor is a potent mitogen for human dermal fibroblasts in an in vitro three-dimensional collagen matrix, the "dermal equivalent." Both cell numbers and DNA synthesis are optimally stimulated by daily doses of 1 ng/ml of the pure human mitogen in the presence of heparin, which binds to, and stabilizes, the protein. Under daily treatment by 1 ng/ml aFGF, the fibroblast mitogenic response is marked but transient, and decreases steadily when fibroblasts mature in the collagen matrix. aFGF mitogenic stimulation also results in a decrease in cellular volume and inhibition of fibroblast-mediated contraction of the collagen gel. Various dosing regimes indicate that, although the greatest mitotic response was generated by daily dosing, nearly optimal responses can also be achieved with either a short duration of early daily dosing or longer-term intermittent treatment.

Cell Count↗
PubMed1991

Photoreactivity of 5-geranoxypsoralen and lack of photoreaction with DNA.

5-Geranoxypsoralen, commonly called bergamottin, a major furocoumarin contained in bergamot oil, is reported in vitro as a highly photoreactive psoralen. In ethanol, it exhibits quite a high triplet state quantum yield (approximately 0.37). The triplet state is involved in subsequent photochemistry which depends on the initial concentration and on the presence of oxygen. In contrast to most psoralens, absorption and fluorescence data suggest that 5-geranoxypsoralen does not interact with DNA in the dark. No UVA-induced interstrand cross-links in DNA were shown.

DNA↗
PubMed1991

Exclusion of linkage between the collagenase gene and generalized recessive dystrophic epidermolysis bullosa phenotype.

Generalized recessive dystrophic epidermolysis bullosa (RDEB) is a severe inherited autosomal disease characterized by dermolytic blister formation. Enhanced collagenase and/or abnormal collagenase have been reported in skin from affected patients, suggesting that collagenase could be responsible for the absence of anchoring fibrils in this disorder. We used a genetic linkage approach to test the hypothesis that this disease is due to a defect in the collagenase gene in nine affected families. Analysis of amplified genomic DNA fragments of the collagenase gene by means of denaturing gradient gel electrophoresis (DGGE) allowed us to detect intragenic polymorphisms, which were subsequently characterized by direct genomic sequencing. Segregation analysis of these polymorphic sites showed exclusion of linkage between the collagenase gene and generalized RDEB phenotype in a family with consanguineous parents and three affected children. However, the possibility of linkage with the collagenase gene in the other eight families tested could not be excluded. The genetic markers described here provide a tool for investigating genetic linkage in other affected families. Overall, our results show that generalized RDEB can be caused by a defect in a gene other than the collagenase gene, and support the hypothesis that the genetic defect lies in abnormal anchoring fibril formation.

Base Sequence↗