Abstract:
:The molecular events involved in both the initiation and development of silicosis are at present poorly defined, although mediators released from macrophages exposed to silica particles are believed to play a role. We have investigated the in vitro production of arachidonic acid (AA) metabolites in adherent bovine alveolar macrophages (BAM) incubated with crystalline silica. BAM were prelabeled with 3H-AA and incubated with 0.5-5.0 mg silica. Lipid metabolites released into the culture medium were analyzed by high-performance liquid chromatography. Simultaneously, lactate dehydrogenase (LDH) was assayed to provide an indication of cell injury. No 5-lipoxygenase metabolites were detected at the lowest silica dose tested (0.5 mg/well), but 5-hydroxyeicosatetraenoic acid (5-HETE) was the major AA metabolite detected between 1.5 and 5.0 mg of silica. A fivefold increase in the production of leukotriene B4 (LTB4) and its two nonenzymatic diastereomers (Isomers I and II) was observed as the silica concentration was increased from 1.0 to 5.0 mg. In contrast, the release of cyclooxygenase products declined with increasing concentrations of silica. LDH release increased in a linear, dose-dependent fashion in the range of silica doses used. The kinetics of eicosanoid release was investigated over a 3-h interval and LDH release was assayed for each time point. Within 15 min following silica addition, a shift to the production of 5-lipoxygenase metabolites was observed, accompanied by a reduction in cyclooxygenase products. This rapid alteration in AA metabolism preceded cell injury as measured by LDH release. These results demonstrate that silica is a powerful stimulator of arachidonic acid metabolism in BAM. Moreover, silica selectively stimulates the 5-lipoxygenase pathway as the dose of silica increases. Our results suggest that dysfunction in arachidonate metabolism could contribute to the pathogenesis of silicosis.
journal_name
Exp Lung Resjournal_title
Experimental lung researchauthors
Englen MD,Taylor SM,Laegreid WW,Liggitt HD,Silflow RM,Breeze RG,Leid RWdoi
10.3109/01902148909069615subject
Has Abstractpub_date
1989-07-01 00:00:00pages
511-26issue
4eissn
0190-2148issn
1521-0499journal_volume
15pub_type
杂志文章abstract:AIM OF THE STUDY:Interleukin (IL)-10 is an anti-inflammatory cytokine, but its role in cigarette smoke (CS)-induced inflammation and chronic obstructive pulmonary disease (COPD) has not been fully elucidated. The purpose of this study was to investigate the effect of IL-10 deficiency on CS-induced pulmonary inflammatio...
journal_title:Experimental lung research
pub_type: 杂志文章
doi:10.3109/01902148.2015.1096315
更新日期:2015-01-01 00:00:00
abstract::Emerging data indicate that endothelial-mesenchymal transition (EndMT) is involved in the pathogenesis of idiopathic pulmonary fibrosis (IPF). A previous study noted that blocking the activity of protein phosphatase 2 A (PP2A) could attenuate EndMT. However, the treatment effects of PP2A inhibitors in pulmonary fibros...
journal_title:Experimental lung research
pub_type: 杂志文章
doi:10.1080/01902148.2020.1774823
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journal_title:Experimental lung research
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doi:10.1080/01902148.2017.1368738
更新日期:2017-10-01 00:00:00
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journal_title:Experimental lung research
pub_type: 杂志文章
doi:10.1080/019021401750069366
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journal_title:Experimental lung research
pub_type: 杂志文章
doi:10.3109/01902149309031730
更新日期:1993-09-01 00:00:00
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journal_title:Experimental lung research
pub_type: 杂志文章
doi:10.3109/01902148.2014.908249
更新日期:2014-08-01 00:00:00
abstract:BACKGROUND AND OBJECTIVE:We have previously reported that N-acetylcysteine (NAC), ambroxol and azithromycin (AZM) (partially) correct the chloride efflux dysfunction in cystic fibrosis bronchial epithelial (CFBE) cells with the ΔF508 homozygous mutation in vitro. METHODS:In the present paper, we further investigated p...
journal_title:Experimental lung research
pub_type: 杂志文章
doi:10.3109/01902148.2014.934411
更新日期:2015-06-01 00:00:00
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journal_title:Experimental lung research
pub_type: 杂志文章
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更新日期:1986-01-01 00:00:00
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journal_title:Experimental lung research
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journal_title:Experimental lung research
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更新日期:2007-08-01 00:00:00
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journal_title:Experimental lung research
pub_type: 杂志文章
doi:10.1080/01902140290092029
更新日期:2002-09-01 00:00:00
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journal_title:Experimental lung research
pub_type: 杂志文章
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更新日期:1987-01-01 00:00:00
abstract:PURPOSE OF THE STUDY:Workers in enclosed hogbarns experience an increased incidence of airway inflammation and obstructive lung disease, and an aqueous hogbarn dust extract (HDE) induces multiple inflammation-related responses in cultured airway epithelial cells. Epidermal growth factor receptor (EGFR) phosphorylation ...
journal_title:Experimental lung research
pub_type: 杂志文章
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更新日期:2018-12-01 00:00:00
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journal_title:Experimental lung research
pub_type: 杂志文章
doi:10.3109/01902149609046037
更新日期:1996-07-01 00:00:00
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journal_title:Experimental lung research
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更新日期:2005-05-01 00:00:00
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更新日期:2004-12-01 00:00:00
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journal_title:Experimental lung research
pub_type: 杂志文章
doi:10.3109/01902148009065460
更新日期:1980-08-01 00:00:00
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journal_title:Experimental lung research
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更新日期:2019-09-01 00:00:00
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journal_title:Experimental lung research
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doi:10.3109/01902149309071077
更新日期:1993-01-01 00:00:00
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journal_title:Experimental lung research
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更新日期:1986-01-01 00:00:00
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journal_title:Experimental lung research
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更新日期:1998-07-01 00:00:00
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journal_title:Experimental lung research
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更新日期:1992-03-01 00:00:00
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journal_title:Experimental lung research
pub_type: 杂志文章
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更新日期:1987-01-01 00:00:00
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journal_title:Experimental lung research
pub_type: 杂志文章
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更新日期:2014-04-01 00:00:00
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journal_title:Experimental lung research
pub_type: 杂志文章
doi:10.3109/01902149509050838
更新日期:1995-09-01 00:00:00
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journal_title:Experimental lung research
pub_type: 杂志文章
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更新日期:1984-01-01 00:00:00
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journal_title:Experimental lung research
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doi:10.3109/01902140903349562
更新日期:2010-05-01 00:00:00
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journal_title:Experimental lung research
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更新日期:1999-06-01 00:00:00
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journal_title:Experimental lung research
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更新日期:2009-10-01 00:00:00
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journal_title:Experimental lung research
pub_type: 杂志文章
doi:10.3109/01902148209069657
更新日期:1982-11-01 00:00:00