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Published on: April 20, 2018
Cyclic Strain and Macrophage-Mediated Transport Govern Micron-Sized PM2.5 Translocation across the Air-Blood Barrier
Yongjian Li1,2, Jinlong Xu1,2, Zujie Gao1,2
1Department of Mechanical Engineering, Tsinghua University, Beijing, 100084, P. R. China.
Abstract:
PM2.5 translocated across the air-blood barrier (ABB) can accumulate in the lungs and extrapulmonary organs, leading to both pulmonary and systemic pathophysiological effects. However, the mechanisms governing the translocation of micron-sized PM2.5 (MPs) remain unclear. Here, a physiologically relevant in vitro ABB model is developed, comprising a triple co-culture system under respiratory-like cyclic strain. Using this platform, it is demonstrated that cyclic stretching enhances dTHP-1 phagocytosis and transmigration, synergistically promoting macrophage-mediated MPs translocation across the ABB in combination with strain-induced disruption of epithelial tight junctions. This cooperative mechanism governs MPs translocation across the ABB and markedly increases the transport of 2 µm particles compared to static conditions. By using scavenger receptor A (SR-A) inhibitors, this process are confirmed to be predominantly driven by macrophage phagocytosis. Furthermore, this study explores the potential fate of particles post-translocation, proposing their subsequent release from macrophages via active lysosomal exocytosis and passive release mediated by cell death. These findings provide new insights into mitigating PM2.5-induced health risks and inform macrophage-assisted pulmonary drug delivery strategies.
Insights
Particulate matter (PM2.5) translocation across the air-blood barrier is enhanced by cyclic stretching, which boosts macrophage phagocytosis and disrupts epithelial barriers. This mechanism increases particle transport and informs strategies for mitigating health risks.
Area of Science:
- Environmental Health Sciences
- Cell Biology
- Respiratory Medicine
Background:
- Particulate matter (PM2.5) translocation across the air-blood barrier (ABB) leads to pulmonary and systemic health issues.
- Mechanisms of micron-sized PM2.5 (MPs) translocation across the ABB are not fully understood.
Purpose of the Study:
- To investigate the mechanisms of MPs translocation across the ABB using a novel in vitro model.
- To elucidate the role of mechanical forces and macrophage activity in MPs transport.
Main Methods:
- Development of a physiologically relevant in vitro ABB model with cyclic strain.
- Utilizing a triple co-culture system to mimic respiratory conditions.
- Employing scavenger receptor A (SR-A) inhibitors to assess macrophage phagocytosis.
Main Results:
- Cyclic stretching enhances macrophage phagocytosis and transmigration, promoting MPs translocation across the ABB.
- Strain-induced disruption of epithelial tight junctions synergizes with macrophage activity.
- The process is predominantly mediated by macrophage phagocytosis via SR-A.
- Particles are released from macrophages through lysosomal exocytosis or passive cell death.
Conclusions:
- A cooperative mechanism involving cyclic stretching and macrophage phagocytosis governs MPs translocation across the ABB.
- This study provides insights into PM2.5 health risks and informs pulmonary drug delivery strategies.
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