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Updated: Jun 11, 2026
Multicellular Human Alveolar Model Composed of Epithelial Cells and Primary Immune Cells for Hazard Assessment
Published on: May 6, 2020
Meconium exposure dependent cell death and apoptosis in human alveolar epithelial cells
Mei-Jy Jeng1, Wen-Jue Soong, Yu-Sheng Lee
1Institute of Emergency and Critical Care Medicine, Department of Pediatrics, School of Medicine, National Yang-Ming University, Taipei, Taiwan, ROC. mjjeng@vghtpe.gov.tw
Abstract:
Alveolar epithelial cells of neonates are directly exposed to aspirated meconium during meconium aspiration syndrome (MAS). This study was designed to investigate the influence of quantity and time of meconium exposure on the cell viability and caspase activity in type II human alveolar epithelial cells. Human alveolar epithelial cells were incubated with human meconium suspension at different concentrations and for different times. Cell viability and DNA fragmentation were investigated together with caspases activity and the amount of Bcl-2 protein present. We found that cell viability was significantly lower in cells exposed to a higher concentration of meconium. This was also true for cells exposed to meconium for longer. Significantly higher DNA fragmentation, an approximately two- to fivefold increase, was observed in cells that had been exposed to higher (5% and 10%) concentration of meconium compared to those treated with lower (0.1% and 1%) concentrations (P < 0.05). The activity of most apoptotic initiators (caspase 2, 8, 9, 10) and effectors (caspase 3, 6) were found to be significantly higher in cells subject to greater meconium exposure compared to cells with no or minor meconium exposure. The level of Bcl-2 was also found to be significantly decreased in meconium-exposed cells (P < 0.05). In conclusion, human meconium would seem to induce direct cell death as well as caspase-dependent apoptosis in alveolar epithelial cells; the amount and period of exposure to meconium are crucial factors in this process. Thus, removing aspirated meconium should alleviate lung cell damage in neonates and improve the outcome with MAS.
Insights
Meconium aspiration syndrome (MAS) damages neonatal lung cells. Higher meconium concentrations and longer exposure times significantly increase cell death and apoptosis, highlighting the importance of meconium removal.
Area of Science:
- Neonatal respiratory distress
- Cellular toxicology
- Apoptosis research
Background:
- Neonatal alveolar epithelial cells face direct meconium exposure during meconium aspiration syndrome (MAS).
- Understanding meconium's impact on lung cells is critical for improving neonatal outcomes.
Purpose of the Study:
- To investigate how meconium quantity and exposure duration affect human alveolar epithelial cell viability and apoptosis.
- To analyze the role of caspases and Bcl-2 protein in meconium-induced cell damage.
Main Methods:
- Human alveolar epithelial cells were exposed to varying meconium concentrations and durations.
- Assays measured cell viability, DNA fragmentation, caspase activity (initiators and effectors), and Bcl-2 protein levels.
Main Results:
- Increased meconium concentration and exposure time significantly reduced cell viability.
- DNA fragmentation rose 2-5 fold with higher meconium concentrations.
- Apoptotic caspase activity (caspase 2, 3, 6, 8, 9, 10) increased, while Bcl-2 protein levels decreased.
Conclusions:
- Human meconium directly induces cell death and caspase-dependent apoptosis in alveolar epithelial cells.
- Meconium concentration and exposure duration are key factors in lung cell damage.
- Timely removal of aspirated meconium is crucial for mitigating neonatal lung injury in MAS.
