Particles induce apical plasma membrane enlargement in epithelial lung cell line depending on particle surface area dose.
BACKGROUND
Airborne particles entering the respiratory tract may interact with the apical plasma membrane (APM) of epithelial cells and enter them. Differences in the entering mechanisms of fine (between 0.1 microm and 2.5 microm) and ultrafine ( <or= 0.1 microm) particles may be associated with different effects on the APM. Therefore, we studied particle-induced changes in APM surface area in relation to applied and intracellular particle size, surface and number.


METHODS
Human pulmonary epithelial cells (A549 cell line) were incubated with various concentrations of different sized fluorescent polystyrene spheres without surface charge (slashed circle fine - 1.062 microm, ultrafine - 0.041 microm) by submersed exposure for 24 h. APM surface area of A549 cells was estimated by design-based stereology and transmission electron microscopy. Intracellular particles were visualized and quantified by confocal laser scanning microscopy.


RESULTS
Particle exposure induced an increase in APM surface area compared to negative control (p < 0.01) at the same surface area concentration of fine and ultrafine particles a finding not observed at low particle concentrations. Ultrafine particle entering was less pronounced than fine particle entering into epithelial cells, however, at the same particle surface area dose, the number of intracellular ultrafine particles was higher than that of fine particles. The number of intracellular particles showed a stronger increase for fine than for ultrafine particles at rising particle concentrations.


CONCLUSIONS
This study demonstrates a particle-induced enlargement of the APM surface area of a pulmonary epithelial cell line, depending on particle surface area dose. Particle uptake by epithelial cells does not seem to be responsible for this effect. We propose that direct interactions between particle surface area and cell membrane cause the enlargement of the APM.
Brandenberger
Christina
C
Institute of Anatomy, University of Bern, Bern, Switzerland. brandenberger@ana.unibe.ch
Rothen-Rutishauser
Barbara
B
Blank
Fabian
F
Gehr
Peter
P
Mühlfeld
Christian
C
D000465:Algorithms; D017209:Apoptosis; D045744:Cell Line, Tumor; D002462:Cell Membrane / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D004305:Dose-Response Relationship, Drug; D004705:Endocytosis; D004847:Epithelial Cells / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D006801:Humans; D016209:Interleukin-8 / Q000378:metabolism; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D050155:Lipogenesis / Q000235:genetics; D008168:Lung / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D018613:Microscopy, Confocal; D046529:Microscopy, Electron, Transmission; D009336:Necrosis; D010316:Particle Size; D052638:Particulate Matter / Q000737:chemistry / Q000378:metabolism / Q000633:toxicity*; D011137:Polystyrenes / Q000737:chemistry / Q000378:metabolism / Q000633:toxicity*; D012815:Signal Processing, Computer-Assisted; D013997:Time Factors; D014158:Transcription, Genetic
C508606:CXCL8 protein, human; D016209:Interleukin-8; D052638:Particulate Matter; D011137:Polystyrenes; D007770:L-Lactate Dehydrogenase