2010
DOI: 10.1111/j.1365-2249.2010.04175.x
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Acute lung injury: apoptosis in effector and target cells of the upper and lower airway compartment

Abstract: SummaryApoptotic cell death has been considered an underlying mechanism in acute lung injury. To evaluate the evidence of this process, apoptosis rate was determined in effector cells (alveolar macrophages, neutrophils) and target cells (tracheobronchial and alveolar epithelial cells) of the respiratory compartment upon exposure to hypoxia and endotoxin stimulation in vitro. Cells were exposed to 5% oxygen or incubated with lipopolysaccharide (LPS) for 4, 8 and 24 h, and activity of caspase-3, -8 and -9 was de… Show more

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Cited by 38 publications
(31 citation statements)
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“…We speculate that the mechanism by which reduced apoptosis correlates with reduced BALT numbers and size is related to a decrease in selfantigen processing. In hypoxia, the pattern of apoptosis induced is cell type-specific in acute hypoxia (27) versus chronic hypoxia (15). Furthermore, the extent of apoptosis is much less obvious compared with MCT.…”
Section: Discussionmentioning
confidence: 91%
“…We speculate that the mechanism by which reduced apoptosis correlates with reduced BALT numbers and size is related to a decrease in selfantigen processing. In hypoxia, the pattern of apoptosis induced is cell type-specific in acute hypoxia (27) versus chronic hypoxia (15). Furthermore, the extent of apoptosis is much less obvious compared with MCT.…”
Section: Discussionmentioning
confidence: 91%
“…LPS has been shown to cause lung injury in rats and can induce apoptosis in lung epithelial cells. [17][18][19] However, no apoptotic effects in static cells, treated with LPS, were observed possibly due to differing experimental conditions such as a shorter time period (24 h instead of 48 h) for incubating cells and always freshly isolated ATII cells. Also the concentrations of LPS (20 mg/mL) was higher and only a moderate increase of apoptotic cells (2-8%) was shown.…”
Section: Discussionmentioning
confidence: 98%
“…5). Both IT LPS (32,53) and VILI (45) have been shown to cause airway injury with increased airway edema associated with increased airway epithelial permeability and apoptosis. Thus it is possible that PDE2A knockdown in this cellular compartment could significantly contribute to the beneficial effects we observed in the overall LPS/VILI insult in mice infected with Ad.PDE2A-shRNA.…”
Section: Discussionmentioning
confidence: 99%