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Biomedical subjects

J F Mornex

Publications and source records attributed to J F Mornex.

123 records · Page 7Linked to original sources
PubMed1979

Elevated serum beta 2-microglobulin levels and C1q-binding immune complexes in sarcoidosis.

Serum beta 2 microglobulin levels were found significantly higher (3.05 +/- 0.98 mg/l) in 32 sarcoidosis patients without renal dysfunction than in normal controls (1.54 +/- 0.22 mg/l). Low levels of C1q-binding immune complexes were detected in 70% of patient's sera, despite the absence of extra-thoracic manifestations. C-reactive protein was detected in 55% of sarcoidosis sera. Neither C1q-binding immune complexes nor C-reactive protein were correlated with beta 2 microglobulin levels. Beta 2 microglobulin raised during relapses and fell under efficient corticosteroid treatment. Beta 2 microglobulin would represent a possible biological marker of disease activity.

Adolescent↗
PubMedDate not supplied

Visna-maedi virus-induced expression of interleukin-8 gene in sheep alveolar cells following experimental in vitro and in vivo infection.

Visna-maedi virus is a lentivirus which causes inflammatory disorders in sheep, including a chronic interstitial lung disease resembling that observed in human immunodeficiency virus type 1 (HIV 1) infection. In view of our previous demonstration of the production of neutrophil chemotactic activity by alveolar macrophages, and given the lymphocytic and neutrophilic nature of the alveolar cell infiltrate in both naturally and experimentally infected animals, we hypothesized that interleukin-8 (IL8) could be a candidate for at least part of the chemotactic activity we described. In this study, we investigated IL8 mRNA expression following visna-maedi virus infection. Northern analysis of total RNA using an ovine IL8-specific probe demonstrated that the IL8 gene is upregulated in alveolar macrophages as a consequence of in vitro infection and in alveolar cells from experimentally infected animals. Using a semi-quantitative RT-PCR method, we showed that various levels of IL8 mRNA are expressed by alveolar cells from infected animals and that they correlate with the intensity of the lesions. In conclusion, visna-maedi virus is able to induce IL8 mRNA expression in sheep alveolar cells. Results from in vivo infected animals suggest that IL8 could play a role in the early build-up of visna-maedi virus-induced lesions.

Animals↗
PubMedDate not supplied

Interstitial lung disease in feline immunodeficiency virus (FIV) infected cats.

Postmortem bronchoalveolar lavage of feline immunodeficiency virus-infected cats indicated an alveolitis process, and histological examination of their lungs confirmed the occurrence of alveolitis, parenchymatous lymphoplasmocytic infiltration and myomatosis. Similar lymphoid interstitial pneumonitis has been described in human and animal lentiviral diseases: lymphocytic interstitial pneumonitis in HIV-1-infected human beings, and maedi in sheep infected by the maedi-visna virus. Such lymphoid interstitial pneumonitis may thus be a common feature of lentiviral infections.

Animals↗
PubMedDate not supplied

Increased expression of tissue factor mRNA and procoagulant activity in ovine lentivirus-infected alveolar macrophages.

To link ovine lentivirus infection to lung tissue damage, we studied the procoagulant response in alveolar macrophages from experimentally infected lambs and in in vitro infected alveolar macrophages. We cloned ovine tissue factor cDNA and analysed its in vitro expression by Northern blotting. Visna-maedi virus induced tissue factor mRNA. In order to correlate this mRNA induction with its cellular function, we analysed macrophage procoagulant activity after in vitro and in vivo infection. The procoagulant activity was increased by interaction with the virus in both cases. Thus, visna-maedi virus-induced expression of tissue factor mRNA was associated with enhanced macrophage procoagulant activity. These findings indicate an active role of alveolar macrophages in the pathogenesis of these inflammatory lung lesions.

Animals↗
PubMedDate not supplied

Activated human monocytes express the c-sis proto-oncogene and release a mediator showing PDGF-like activity.

Current ideas about the mechanism of wound healing and the pathogenesis of atherosclerosis, pulmonary fibrosis and hepatic fibrosis suggest a central role for the mononuclear phagocyte in attracting and/or stimulating the proliferation of mesenchymal cells. We demonstrate here that activated human blood monocytes, but not resting monocytes, release a mediator that attracts smooth muscle cells and cooperates with other mediators to stimulate fibroblast proliferation. This mediator is very similar to platelet-derived growth factor (PDGF): its chromatographic properties and chemical stability are similar to those of PDGF, it competes with 125I-PDGF for binding to fibroblasts and it immunoprecipitates with anti-PDGF antibodies. In parallel, stimulated monocytes, but not resting monocytes, express the c-sis proto-oncogene, a gene coding for one of the PDGF chains, consistent with the concept that expression of the c-sis proto-oncogene may be involved in the ability of mononuclear phagocytes to modulate the accumulation of mesenchymal cells.

Gene Expression Regulation↗
PubMedDate not supplied

Immortalized goat milk epithelial cell lines replicate CAEV at high level.

Primary milk epithelial cells were isolated from CAEV-uninfected goats and three cell lines designated TIGMEC-1, TIGMEC-2 and TIGMEC-3 were established. The three cell lines retained their morphological characteristics of epithelial cells and expressed specific epithelial cytokeratin marker as well as the immortalizing SV40 large T antigen. The kinetics of growth of TIGMEC1, TIGMEC2 and TIGMEC3 cell lines showed a doubling time of 24-48 hours while the parental cell lines became senescent after the passage 6 in cell culture. Like the parental primary cells, the three cell lines were found to be highly sensitive to CAEV-pBSCA, an infectious molecular clone of CAEV-CO strain, and to a French isolate CAEV-3112. TIGMEC cell lines infected with CAEV-pBSCA became chronically infected producing high virus titers in absence of cytopathic effects. These cell lines may be useful for study of the possible physiological alterations in mammary epithelial cells infected with small ruminant lentiviruses and their consequences on milk quality. On an other hand, these cell lines can be used to study their role in virus transmission and pathogenesis.

Animals↗
PubMedDate not supplied

Infection of primary cultures of mammary epithelial cells by small ruminant lentiviruses.

The caprine arthritis-encephalitis virus (CAEV) and Visna Maedi virus cause persistent infections with long latent periods and induce degenerative and chronic inflammatory lesions of the central nervous system, joints, lungs and udder. Monocyte/macrophage lineage is the main target cell for CAEV and Visna Maedi virus but we speculate that mammary epithelial cells may also be infected. Primary cultures of milk cells, mammary tissues of experimentally and naturally infected goats and ewes were used. Primary cultures of mammary tissue from ewes and goats were infected with the CAEV Cork strain. The lentiviral infection of the primary culture was demonstrated by a typical cytopathic effect in mammary epithelial cells and the presence of an infectious virus in coculture with permissive fibroblasts. To identify the epithelial cells in explants and demonstrate the antigenic expression of CAEV, primary cultures were immunostained with polyclonal anti-keratin and monoclonal anti-CAEV p30. Colocalisation studies under a UV fluorescence microscope and by epifluorescence microscopy showed the expression of specific viral antigens in mammary epithelial cells from the eight animals used. Infected mammary epithelial cells may act as a reservoir for the virus which may play an important role in the virus dissemination and in the pathogenesis of the mammary lentiviral disease.

Animals↗
PubMedDate not supplied

Bronchoalveolar lavage in radiation pneumonitis.

Bronchoalveolar lavage (BAL) was carried out in six patients with radiation pneumonitis, the early radiation-induced lung damage that usually leads to radiation fibrosis. Protein analysis by immuno-electrophoresis and polyacrylamide gel electrophoresis of BAL fluid revealed leakage of circulatory proteins, including high molecular weight components. Cell count of BAL fluid showed an increased number of lymphocytes; these proved to be activated on cell cycle analysis in one patient. Collagenolytic activity, assessed by degradation of radiolabelled type I human collagen, was present in BAL fluid of all six patients. The following mechanisms are therefore considered to participate in the pathogenesis of radiation-induced lung damage: 1) permeability oedema, which led to acute respiratory distress syndrome in one case of hyperacute radiation pneumonitis, 2) lymphocyte alveolitis possibly perpetuated by activated lymphocytes, and 3) release of collagenolytic enzymes in alveolar structures contributing to fibrotic processes.

Bronchi↗
PubMedDate not supplied

Maedi-visna virus infection in sheep: a review.

The maedi-visna virus (MVV) is classified as a lentivirus of the retroviridae family. The genome of MVV includes three genes: gag, which encodes for group-specific antigens; pol, which encodes for reverse transcriptase, integrase, RNAse H, protease and dUTPase and env, the gene encoding for the surface glycoprotein responsible for receptor binding and entry of the virus into its host cell. In addition, analogous to other lentiviruses, the genome contains genes for regulatory proteins, i.e. vif, rev and tat. The coding regions of the genome are flanked by long terminal repeats (LTR) which play a crucial role in the replication of the viral genome and provide binding sites for cellular transcription factors. The organs targeted by MVV are, in descending order of importance, the lungs, mammary glands, joints and the brain. In these organs, the virus replicates in mature macrophages and induces slowly progressing inflammatory lesions containing B and T lymphocytes. The clinical signs of MVV infection, i.e. dyspnea, loss of weight, mastitis and arthritis, are related to the location of these lesions. Infection with MVV induces the formation of antibodies which can be detected by agar gel immunodiffusion, ELISA and the serum neutralization assay. As neither antiviral treatment nor vaccination is available, diagnostic tests are the backbone of most of the schemes implemented to prevent the spread of MVV. However, since current serological assays are still lacking in sensitivity and specificity, molecular biological methods are being developed permitting the detection of virus in peripheral blood, milk and tissue samples. Future research will have to focus on both the development of new diagnostic tests and a better understanding of the pathogenesis of MVV infection.

Animals↗