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Biomedical subjects

A Venet

Publications and source records attributed to A Venet.

At least 55 records · Page 3Linked to original sources
PubMed1988

Serum HIV antigen and anti-P24-antibodies in 200 HIV seropositive patients: correlation with CD4 and CD8 lymphocyte subsets.

Serum HIV (P24) antigen (Ag) measured by an antigen capture ELISA (Abbott) and anti-P24-antibodies (Abs) measured by a competitive ELISA (Abbott) and by Western Blot (Dupont de Nemours) analysis were correlated with lymphocyte subsets (CD4 and CD8) in 174 HIV seropositive patients without AIDS (non-AIDS) and 26 with AIDS. In the non-AIDS group, 27% of the patients were anti-P24-Ab negative and 21% were Ag positive while in the AIDS group these figures were 62% and 54% respectively (P less than 0.001). Overall, a significant correlation exists between the Ab-Ag profile and the CD4 cell count: the percentage of patients with anti-P24-Ab positive and Ag negative decreases from 90% for patients with more than 900 CD4 cells/microliter to 21% for patients with 100 and less CD4 cells/microliter; on the contrary, the percentage of patients with anti-P24-Ab negative and Ag positive increases from 0% over 800 CD4 cells to 53% under 100 CD4 cells/microliter. A weak correlation may also exist with the CD8 cell count. The subgroup of patients with 1,000 or more CD8 cells/microliter have a higher (but not significant) percentage of subjects with Ag positive and anti-P24-Ab negative than the subgroup with less than 1,000 CD8 cells/microliter. A short-term longitudinal study (mean follow-up: 1 year) was performed on 80 non-AIDS subjects: 77% (10/13) of those who had a CD4 cell decrease (greater than 30%) were initially Ag positive, while only 21% (14/67) of those without a decrease were Ag positive at the beginning (P less than 0.1). Although the relative weight and individual predictive value of each of these parameters need to be classified, they are probably the best biological markers currently available for monitoring clinical trials with experimental drugs.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Pulmonary complications of intravesical Bacille Calmette-Guérin immunotherapy.

Lungs have rarely been reported to be affected by any side effects of BCG therapy. Interstitial pneumonitis, though, is known to occur under such circumstances, but its pathogenesis is still debated between an infectious and a hypersensitivity mechanism. We report here 3 cases of pulmonary complications of BCG therapy evaluated by bronchoalveolar lavage (BAL). Cellular data obtained from all 3 patients were characterized by a markedly increased alveolar lymphocytosis. The T4/T8 ratio was elevated compared with that in normal subjects and with the T4/T8 ratio of circulating lymphocytes. Furthermore, alveolar lymphocytes were highly sensitized to PPD, as evaluated by their proliferation and their production of interleukin 2 in the presence of PPD. Mycobacteria were not found in the 3 patients. We conclude that interstitial pneumonitis occurring during BCG therapy could be explained by a hypersensitivity phenomenon, leading to an intense immune and lymphocyte-mediated response within involved organs.

Adult↗
PubMed1987

Bronchoalveolar lavage in amiodarone pneumonitis. Cellular abnormalities and their relevance to pathogenesis.

To investigate the contribution of direct cytotoxicity and immune-mediated hypersensitivity to the pathogenesis of amiodarone pneumonitis, we evaluated cells recovered by bronchoalveolar lavage from 13 patients with amiodarone pneumonitis. Alveolar macrophages from all patients contained two types of abnormal inclusions: small clear vacuoles and large phagolysosomes containing phospholipid in lamellar structures, abnormalities previously attributed to direct cytotoxicity from amiodarone. However, these changes were always associated with abnormalities in the numbers and types of immune and inflammatory cells present in the lower respiratory tract, which closely resemble those seen in hypersensitivity pneumonitis associated with inhaled antigens. Following discontinuation of amiodarone and institution of corticosteroid therapy, clinical improvement correlated with a return toward normal in the pattern of inflammatory cells present in the lung, although alveolar macrophages continued to display evidence of drug-induced cytotoxicity. These findings support the possibility that a cell-mediated immune response usually plays a role in the pathogenesis of amiodarone pneumonitis, although direct cytotoxicity may predispose these patients to the development of this abnormal immune response.

Aged↗
PubMed1986

Persistent high alveolar lymphocytosis as a predictive criterion of chronic pulmonary sarcoidosis.

A homogeneous population of 73 sarcoidosis patients with recent onset sarcoidosis, no smoking habits, and no previous treatments was serially evaluated in a study of the spontaneous evolution of sarcoidosis. This evaluation comprised clinical, radiographic, biological, and functional assessments as well as assessments of fluids recovered by BAL. We determined the natural history of alveolar lymphocytosis in early stage sarcoidosis and the predictive value of such lymphocytosis for the outcome of the disease. We focused on the outcome at 2 years because it is the usual time of spontaneous recovery; after 2 years the disease enters the chronic phase, and more complications are likely to occur. We found that the initial lymphocytosis observed during the very early stages of the disease had no predictive value for the outcome. Conversely, the persistence of a high alveolar lymphocytosis within the first year of evolution is strongly correlated to a nonrecovery at 2 years, and thus to a chronic phase of sarcoidosis.

Adult↗
PubMed1986

Human alveolar macrophage subpopulations isolated on discontinuous albumin gradients. Cytological data in normals and sarcoid patients.

Cells recovered by bronchoalveolar lavage (BAL) from ten subjects (five normals and five sarcoid patients) were centrifuged on discontinuous albumin gradients to study alveolar macrophage (AM) heterogeneity. The gradient was made with nine bovine albumin concentrations (from 8 to 30%). After centrifugation (4000 X g) cells were recovered from the interfaces. The majority of AM was recovered in upper and medium layers with AM purity reaching 90-100% in upper layers, while lymphocytes and granulocytes were found in lower layers. Alveolar macrophage morphology was different along the gradient. Large cytoplasmic vacuoles were found in AM from upper layers. Alveolar macrophage cytoplasmic diameters decreased from the top to the bottom of the gradient, but AM from sarcoid patients appeared larger than AM from normals. Alveolar macrophage nucleo-cytoplasmic ratios increased from top to bottom, but were lower in sarcoid patients than in normals. Alveolar macrophage peroxidase activity was rare (0.5-2% of AM) but reached a higher proportion in upper and lower layers.

Adult↗
PubMed1986

Human alveolar macrophage subpopulations isolated on discontinuous albumin gradients: functional data in normals and sarcoid patients.

Cells recovered by bronchoalveolar lavage from seven normals and seven sarcoid patients were centrifuged on discontinuous bovine albumin (BSA) gradients to study alveolar macrophage (AM) heterogeneity. The gradient was made with nine BSA concentrations from 8 to 30%. After centrifugation, the cells were recovered from the nine interfaces, named a to i. The majority of the AM was recovered from layers b to g. Regulatory activity of AM subpopulations was tested on mitogen-induced blood mononuclear cells (BMC) proliferation: autologous BMC were cocultured with AM from the different layers; 16-h culture supernatants of AM subfractions were added to allogeneic BMC cultures from normal donors. In the autologous assay, AM from the middle layers exhibited a stimulatory activity in normals and even more in sarcoid patients, while AM from the upper layers showed an inhibitory activity in normals but a stimulatory activity in sarcoid patients. In the allogeneic assay, a suppressive effect was found in culture supernatants from normal AM. On the other hand, in sarcoid patients, culture supernatants were less inhibiting, but the inhibitory activity was in both cases maximal in b. These results confirm functional heterogeneity of human AM, and demonstrate that the AM subpopulations differ between normals and sarcoid patients.

Adult↗
PubMed1985

Bronchoalveolar lavage in sarcoidosis.

Bronchoalveolar lavage (BAL) was performed in 1,188 patients suffering from sarcoidosis. After technical considerations, the authors analyze the results of BAL from a practical point of view concerning its value for the diagnosis of sarcoidosis and its prognostic value and its value for the selection of therapy, particularly for the decision as to steroid treatment. BAL helps in the diagnosis of sarcoidosis, but is not specific enough to provide this diagnosis on its own. The persistence of high alveolar lymphocytosis within the first year of evolution is strongly correlated with nonrecovery from pulmonary sarcoidosis at 2 years and thus with the evolution towards a chronic phase of the disease. On the other hand, BAL can provide basic information for a better understanding of the disease and permits immunocompetent cells and soluble factors to be recovered from the lung, which is useful for immunological studies.

Adult↗
PubMed1985

Enhanced alveolar macrophage-mediated antigen-induced T-lymphocyte proliferation in sarcoidosis.

Expansion of T-lymphocyte numbers is a characteristic feature of the alveolitis of pulmonary sarcoidosis. One mechanism that may influence the numbers of T-lymphocytes in the lung is the process of antigen presentation in which alveolar macrophages, in the presence of antigen, induce T-lymphocytes to replicate. To evaluate this process in sarcoidosis, alveolar macrophages were obtained by bronchoalveolar lavage, pulsed with tetanus toxoid, and co-cultured with purified autologous T cells. Strikingly, antigen-pulsed alveolar macrophages from sarcoid patients induced more than a twofold increase in autologous T-lymphocyte proliferation compared with the response seen using cells from normal or patients with idiopathic pulmonary fibrosis (P less than 0.001), all comparisons). In contrast, when monocytes were used as the antigen presenting cell, no significant differences were observed in T cell proliferation induced by antigen among the three groups. The enhanced T-lymphocyte proliferation induced by sarcoid alveolar macrophages was not dependent on the compartment from which the T cells were derived, and was independent of the specific antigen used. One possible explanation for augmented antigen presentation seen in sarcoid is that an increased percentage of sarcoid alveolar macrophages express HLA-DR or HLA-DS surface antigens. However, most normal and sarcoid alveolar macrophages express HLA-DR and HLA-DS surface antigens, and the percentage of macrophages expressing these antigens was not significantly different in the two groups. Thus, while the mechanisms of the enhanced antigen presentation in the sarcoid lung are unknown, the process of antigen-driven, alveolar macrophage-modulated lung T cell proliferation may explain, at least in part, the expansion of lung T-lymphocyte numbers that characterizes this disease.

Adolescent↗
PubMed1985

[Pneumopathies caused by hypersensitivity to amiodarone and associated nephropathies. Study by alveolar lavage].

Four cases of amiodarone-induced restrictive, hypoxaemic lung disease are described. The cumulative dosages of amiodarone were relatively low (30 to 100 g). Alveolar lavage studies showed a lymphocytosis and study of the lymphocytic sub-populations showed an increase in the OKT8 group, and an inversion of the OKT4/OKT8 ratio. The outcome was favourable on withdrawal of amiodarone and steroid therapy. The immunological origin of this form of lung disease was confirmed. Two patients had renal failure; in the first case, hypercalcaemia, hyperphosphoremia and renal calcification were observed. The second patient had endo- and extracapillary glomerulonephritis with C3 deposits and circulating immune complexes. Renal failure regressed in both cases on withdrawal of amiodarone and with steroid therapy.

Acute Kidney Injury↗
PubMed1984

Eosinophil-mediated injury to lung parenchymal cells and interstitial matrix. A possible role for eosinophils in chronic inflammatory disorders of the lower respiratory tract.

Eosinophils are a common component of the inflammation of the lower respiratory tract that characterizes the interstitial lung disorders. Bronchoalveolar lavage analyses (n = 680) of 251 patients with interstitial lung disease demonstrated that eosinophils represented greater than 5% of the effector cells comprising the alveolitis in 20% of all lavages. In contrast, lavage of normal individuals (n = 117) showed that eosinophils were never greater than 5% of the total effector cells recovered. To evaluate a possible role for eosinophils in mediating some of the cellular and connective tissue matrix derangements of the lung parenchyma found in interstitial disease, eosinophils were evaluated for the presence of proteases capable of cleaving connective tissue proteins found in the lung and for the ability to mediate cytotoxicity to lung parenchymal cells. Evaluation of guinea pig and human eosinophils demonstrated that eosinophil granules contained a collagenase that specifically cleaved human collagen types I and III, the two major connective tissue components of the human lung parenchyma. In contrast, the eosinophil did not contain an elastase or a nonspecific neutral protease. The eosinophil collagenase appeared to be a metalloprotease, as it was inhibited by ethylenediaminetetraacetate but not by phenylmethanesulfonyl-fluoride or alpha 1-antitrypsin. The eosinophil also has the capacity to injure lung parenchymal cells. Without further stimulation, eosinophils purified from peritoneal exudates of guinea pigs demonstrated spontaneous cytotoxicity for human lung fibroblasts (HFL-1), cat lung epithelial cells (AK-D) and rat lung mesothelial cells (I6B). Under identical conditions, the epithelial cells were more sensitive to eosinophil-mediated cytotoxicity than the fibroblasts or mesothelial cells (P less than 0.01), consistent with the clinical observation that in the interstitial disorders, the alveolar epithelial cells are damaged more commonly than fibroblasts or pleural cells. The eosinophil-mediated cytotoxicity could be partially inhibited by the antioxidants catalase and dimethylsulfoxide suggesting that toxic oxygen radicals play a role in mediating the cellular damage. Importantly, eosinophils purified from bronchoalveolar lavage of human interstitial lung disease also demonstrated spontaneous cytotoxicity for lung epithelial cells. These observations demonstrate that eosinophils are frequent participants of the alveolitis of the interstitial lung disorders and suggest that these cells have the potential to damage the parenchymal cells and collagen matrix of the lower respiratory tract.

Animals↗