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J Masliah

Publications and source records attributed to J Masliah.

44 records · Page 3Linked to original sources
PubMed1987

Effects of oxygen-derived free radicals on type II pneumocytes in primary culture.

After a brief review of oxygen-derived free radicals formation, cellular antioxidant equipment, and in vivo oxidant lung injury, the model of type II pneumocytes in primary culture is described with its characteristics and limitations. This model has been used to study either the in vivo or the in vitro effects of free radicals: the resistance of type II cells isolated from animals exposed to oxidants may be explained by their higher level of anti-oxidant enzymes. In contrast, type II cells isolated from control animals do not develop a resistance to the toxic effects on an in vitro exposure to free radicals. This discrepancy might be the result of a possible interaction of alveolar macrophages or fibroblasts with type II cells, which remains to be explored.

Adaptation, Physiological↗
PubMed1986

Changes induced by PAF-acether in diacyl and ether phospholipids from guinea-pig alveolar macrophages.

The release and the mobilization of arachidonic acid from guinea-pig alveolar macrophages labeled with [1-14C]arachidonic acid for short (1 h) and long (18 h) periods and stimulated with PAF-acether (1-alkyl-2-acetyl-sn-glycero-3-phosphocholine) was studied. After short labeling periods arachidonic acid was primarily incorporated into alkylacyl- and diacylglycerophosphocholine (alkylacylGPC, diacylGPC) and glycerophosphoinositol (GPI), whereas after long labeling periods arachidonic acid was mainly incorporated into alkenylacylglycerophosphoethanolamine (alkenylacylGPE). In macrophages labeled for 1 h, PAF-acether (1 microM) induced a significant decrease in the amount of arachidonic acid esterified into diacyl- and alkylacylGPC and GPI, as well as a significant increase of arachidonate transferred into alkenylacylGPE. No significant decrease in arachidonate esterified in GPC fractions and in GPI was induced by PAF-acether in macrophages labeled for 18 h, whereas the increased transfer of the fatty acid into alkenylacylGPE was still measurable. This study shows that PAF-acether induces the release and the mobilization of newly incorporated arachidonic acid in alveolar macrophages. When cells are labeled for long periods and the majority of arachidonic acid is retained in ether-linked phospholipids, no PAF-acether-induced release of arachidonate was obtained, whereas its transfer was maintained.

Animals↗
PubMed1983

Phospholipase activities of bronchoalveolar lavage fluid in rat Pneumocystis carinii pneumonia.

Respiratory distress, main clinical symptom of P. carinii pneumonia, is unexplained. We wondered if it could be linked with a lung surfactant anomaly. We have shown in the bronchoalveolar fluid lavage of P. carinii-infected rats: a very significant decrease of the phospholipid content; a lowering of the phospholipid/protein ratio; and an increase in phospholipase activities, partly due to the activation of an inactive phospholipase into the active form. We conclude that, in P. carinii-infected rats, there is an increased catabolism of lung surfactant.

Animals↗
PubMed1981

Phospholipase and prophospholipase activities in bronchoalveolar lavage fluid in severe acute pulmonary disease with or without ARDS.

Bronchoalveolar lavages were performed in 21 patients undergoing mechanical ventilation: Group I: coma due to sedative overdose (11 cases), without pulmonary impairment, serving as control group; Group II: severe acute pulmonary disease without ARDS (5 cases); Group III: patients with ARDS (5 cases). In the recovered fluid we measured: total proteins (P) and phospholipids (PL), phospholipasic (PLase) and prophospholipasic (PPLase) activities. In ARDS group, considerable increase of P, (p less than 0.001), and a doubling of PL (p less than 0.02) was found. Total PLase activity was present in all three groups, with a higher mean level in Group III (p less than 0.01). PPLase activities were low or undetectable in four patients of this group. PLase/PL ratio was increased in acute respiratory insufficiency, with or without ARDS, suggesting an increase of surfactant catabolism. The decrease of this ratio when pulmonary function improved, or its increase after deterioration suggest that it is related to changes of surfactant.

Acute Disease↗
PubMedDate not supplied

Decreased phosphatidyl choline content in bronchoalveolar lavage fluids of children with bronchopulmonary dysplasia: a preliminary investigation.

Bronchoalveolar lavage (BAL) was performed on 12 infants who had recovered from neonatal acute respiratory failure and on 12 patients with bronchopulmonary dysplasia (BPD) in order to evaluate the concentration of phosphatidyl choline (PC) in BAL fluid. These two groups were similar at birth (mean birth weight: 1,980 and 1,750 g, respectively; mean gestational age: 33.4 and 32.1 weeks respectively). Mechanical ventilation based on oxygen requirement lasted longer in the group with BPD. BAL was performed at the end of the first year of life (at 8.5 and 10.3 months, respectively) and the results were compared to control values (from infants of the same age without neonatal disease). Whereas the protein concentration in BAL fluid was similar in the two groups, a dramatic decrease of the BAL PC was found in BPD: The mean values of BAL-PC over protein ratio were 0.9 in the group without pulmonary sequelae and 0.3 in the group with BPD. These preliminary results suggest an impairment of the pulmonary surfactant metabolism in this chronic lung disease following neonatal acute respiratory failure.

Bronchopulmonary Dysplasia↗
PubMedDate not supplied

Secretory non-pancreatic phopholipase A2 in severe sepsis: relation to endotoxin, cytokines and thromboxane B2.

Circulatory secretory non-pancreatic phospholipase A2 (snp-PLA2) was measured prospectively at the onset (day 0) of severe sepsis in 52 patients as well as on day 1 and 2 in 25 patients, in order to answer two questions: 1) does the snp-PLA2 plasma concentration differ according to the type and severity of infection? 2) what is the relation between snp-PLA2 and other mediators involved in severe sepsis, such as endotoxin, cytokines (TNF alpha, IL-1 beta, IL-6) and thromboxane B2 (the stable metabolite of thromboxane A2)? On day 0, the snp-PLA2 circulatory level was 78 +/- 17 nmol/min/ml in patients with severe sepsis as compared to 3.5 +/- 2 nmol/min/ml in 40 healthy volunteers. There was no statistical difference according to the outcome, the presence of shock, or the type of infection on day 0. However, snp-PLA2 remained elevated or even increased in patients who ultimately died, while it decreased in survivors (p = 0.01 by ANOVA). The cytokine profiles during the 2-day follow-up were similar to that of snp-PLA2, but the differences were not statistically significant between survivors and non-survivors. No correlation was found between snp-PLA2 and other mediators for either initial or peak values.

Adult↗
PubMedDate not supplied

G proteins as biological targets for anti-allergic drugs?

The inhibiting effect of the H1 antihistamine cetirizine on the release of mediators (LTB4, arachidonic acid and phospholipase A2) was measured in different cells in vitro (human PMN, deltaF508 cells, chinese hamster ovary cells and rabbit chondrocytes) using different agonists (fMLP, NaF, calcium ionophore A 23187, bradykinin, adrenaline and IL-1). It was shown that physiological concentrations of the drug inhibited the release when activation of receptor-coupled G proteins was involved. By contrast, there was no inhibiting effect of cetirizine when the release was induced by a calcium ionophore which bypasses the G proteins coupled to cell membrane receptors.

Animals↗