Acetaminophen decreases intracellular glutathione levels and modulates cytokine production in human alveolar macrophages and type II pneumocytes in vitro

2005 ◽  
Vol 37 (8) ◽  
pp. 1727-1737 ◽  
Author(s):  
Svetlana Dimova ◽  
Peter H.M. Hoet ◽  
David Dinsdale ◽  
Benoit Nemery
2000 ◽  
Vol 59 (11) ◽  
pp. 1467-1475 ◽  
Author(s):  
Svetlana Dimova ◽  
Peter H.M Hoet ◽  
Benoit Nemery

2010 ◽  
Vol 56 (3) ◽  
pp. 229-235 ◽  
Author(s):  
Benquan Wu ◽  
Wenxian Zhang ◽  
Jing Huang ◽  
Hui Liu ◽  
Tiantuo Zhang

Panton–Valentine leukocidin (PVL) is associated with rare cases of necrotizing pneumonia that occur in otherwise healthy individuals. Human alveolar macrophages (HAMs) are major effector cells in host defense against infections. However, the impact of PVL on HAMs is uncertain. We evaluated the role of PVL in cytotoxicity and production of inflammatory cytokines secreted by HAMs. HAMs were purified from bronchoalveolar lavage fluid. Recombinant PVL (rPVL) was used in the study to interfere with HAM apoptosis and cytokine production in vitro. Hoechst 33342 fluorescence staining, transmission electron microscopy examination, and flow cytometry indicated that rPVL (10 nmol/L) treatment resulted in HAMs with markedly apoptotic characteristics, and HAMs treated with rPVL at 100 nmol/L showed clear indication of necrosis. A treatment of rPVL at 10 nmol/L elicited the secretion of IL-10 by HAMs relative to untreated control cells, but there was a slight decrease in the constitutive secretion of tumor necrosis factor (TNF)-α. Our results indicate that PVL-treated samples decreased HAM viability, leading to apoptosis at low concentrations and necrosis at high concentrations. In addition, PVL-treated cells released increased amounts of IL-10 and decreased amounts of TNF-α under apoptosis-inducing concentrations. Therefore, we speculated that PVL could play a negative role in HAM function at lower concentrations.


2000 ◽  
Vol 162 (1) ◽  
pp. 2-9 ◽  
Author(s):  
G. Roesems ◽  
P.H.M. Hoet ◽  
D. Dinsdale ◽  
M. Demedts ◽  
B. Nemery

1996 ◽  
Vol 51 (2) ◽  
pp. 150-156 ◽  
Author(s):  
Marli Maria Knorst ◽  
Klaus Kienast ◽  
Joachim Müller-Quernheim ◽  
Rudolf Ferlinz

1998 ◽  
Vol 76 (7-8) ◽  
pp. 721-727 ◽  
Author(s):  
M W Bolt ◽  
W J Racz ◽  
J F Brien ◽  
T M Bray ◽  
T E Massey

Treatment of cardiac dysrhythmias with the iodinated benzofuran derivative amiodarone (AM) is limited by pulmonary toxicity. The susceptibilities of different lung cell types of male Golden Syrian hamsters to AM-induced cytotoxicity were investigated in vitro. Bronchoalveolar lavage and protease digestion to release cells, followed by centrifugal elutriation and density gradient centrifugation, resulted in preparations enriched with alveolar macrophages (98%), alveolar type II cells (75-85%), and nonciliated bronchiolar epithelial (Clara) cells (35-50%). Alveolar type II cell and Clara cell preparations demonstrated decreased viability (by 0.5% trypan blue dye exclusion) when incubated with 50 µM AM for 36 h, and all AM-treated cell preparations demonstrated decreased viability when incubated with 100 or 200 µM AM. Based on a viability index ((viability of AM-treated cells ÷ viability of controls) × 100%), the Clara cell fraction was significantly (p < 0.05) more susceptible than all of the other cell types to 50 µM AM. However, AM cytotoxicity was greatest (p < 0.05) in alveolar macrophages following incubation with 100 or 200 µM AM. There was no difference between any of the enriched cell preparations in the amount of drug accumulated following 24 h of incubation with 50 µM AM, whereas alveolar macrophages accumulated the most drug during incubation with 100 µM AM. Thus, the most susceptible cell type was dependent on AM concentration. AM-induced cytotoxicity in specific cell types may initiate processes leading to inflammation and pulmonary fibrosis.Key words: amiodarone, susceptibility, alveolar macrophage, accumulation.


Thorax ◽  
1996 ◽  
Vol 51 (8) ◽  
pp. 781-786 ◽  
Author(s):  
B. Melloni ◽  
O. Lesur ◽  
T. Bouhadiba ◽  
A. Cantin ◽  
M. Martel ◽  
...  

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