scholarly journals THE EFFECT OF ASBESTOS AND STONE-WOOL FIBRES ON SOME CHEMOKINES AND REDOX SYSTEM OF PULMONARY ALVEOLAR MACROPHAGES AND PNEUMOCYTES TYPE II

2005 ◽  
Vol 149 (2) ◽  
pp. 357-361 ◽  
Author(s):  
Erzsebet Tatrai ◽  
Marta Brozik ◽  
Zuzana Kovacikova ◽  
Magdolna Horvath
1989 ◽  
Vol 257 (3) ◽  
pp. C579-C587 ◽  
Author(s):  
N. A. Saunders ◽  
J. K. McGeachie ◽  
K. F. Ilett ◽  
R. F. Minchin

The lungs have a high polyamine transport capability, and the type II pneumocyte has recently been identified as a major site of putrescine uptake and localization (N. A. Saunders, P. J. Rigby, K. F. Ilett, and R. F. Minchin. Lab. Invest. 59: 380-386, 1988). However, recent evidence suggests that multiple polyamine transport systems exist. In the present study, localization of spermidine uptake in rabbit lung was investigated. Although [14C]spermidine was rapidly accumulated by lung slices, it was not significantly metabolized, and no efflux of the accumulated polyamine was apparent. Autoradiographs prepared after [3H]spermidine transport revealed a localization of uptake activity to cells identified by electron microscopy as type II pneumocytes. Spermidine uptake occurred in all type II cells examined and thus appeared to be a characteristic function of this cell type. In contrast, spermidine uptake was virtually absent in the major airways and blood vessels, whereas moderate uptake was associated with pulmonary alveolar macrophages and alveolar tissue. Subsequent purification and culture of type II pneumocytes showed these cells to have significant polyamine uptake activity. In addition, spermidine uptake activity was positively correlated with the proportion of type II cells present at the various stages of their purification. In other studies, cultured pulmonary alveolar macrophages possessed similar uptake activity to that of cultured type II cells. Combined, these data suggest that both type II cells and pulmonary alveolar macrophages may represent major sites of spermidine uptake in vivo. We also suggest that the transport of polyamines by type II cells may reflect a critical role for polyamines in a characteristic function of this cell type.


2005 ◽  
Vol 26 (1) ◽  
pp. 16-24 ◽  
Author(s):  
Erzsébet Tátrai ◽  
Márta Brozik ◽  
Ágnes Drahos ◽  
Zuzana Kováčiková ◽  
Éva Six ◽  
...  

1987 ◽  
Vol 21 (1-2) ◽  
pp. 15-26 ◽  
Author(s):  
Elaine S. Wright ◽  
David M. White ◽  
Alexandra N. Brady ◽  
Linda C. Li ◽  
James B. D'Arcy ◽  
...  

2016 ◽  
Vol 22 (8) ◽  
pp. 682-695 ◽  
Author(s):  
Qin Yang ◽  
Maren J Pröll ◽  
Dessie Salilew-Wondim ◽  
Rui Zhang ◽  
Dawit Tesfaye ◽  
...  

Pulmonary alveolar macrophages (AMs) are important in defense against bacterial lung inflammation. Cluster of differentiation 14 (CD14) is involved in recognizing bacterial lipopolysaccharide (LPS) through MyD88-dependent and TRIF pathways of innate immunity. Sulforaphane (SFN) shows anti-inflammatory activity and suppresses DNA methylation. To identify CD14 epigenetic changes by SFN in the LPS-induced TRIF pathway, an AMs model was investigated in vitro. CD14 gene expression was induced by 5 µg/ml LPS at the time point of 12 h and suppressed by 5 µM SFN. After 12 h of LPS stimulation, gene expression was significantly up-regulated, including TRIF, TRAF6, NF-κB, TRAF3, IRF7, TNF-α, IL-1β, IL-6, and IFN-β. LPS-induced TRAM, TRIF, RIPK1, TRAF3, TNF-α, IL-1β and IFN-β were suppressed by 5 µM SFN. Similarly, DNMT3a expression was increased by LPS but significantly down-regulated by 5 µM SFN. It showed positive correlation of CD14 gene body methylation with in LPS-stimulated AMs, and this methylation status was inhibited by SFN. This study suggests that SFN suppresses CD14 activation in bacterial inflammation through epigenetic regulation of CD14 gene body methylation associated with DNMT3a. The results provide insights into SFN-mediated epigenetic down-regulation of CD14 in LPS-induced TRIF pathway inflammation and may lead to new methods for controlling LPS-induced inflammation in pigs.


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.


Nature ◽  
1973 ◽  
Vol 245 (5421) ◽  
pp. 150-152 ◽  
Author(s):  
S. C. SODERLAND ◽  
Y. NAUM

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