| Die Interaktion zwischen pulmonalem Surfactant und inhalierbaren Partikeln (2009) | |||||||||||
Abstract | |||||||||||
| Pulmonary surfactant covers the alveoli and reduces surface tension at the air liquid interface, thus maintaining lung function and preventing alveolar collapse. Furthermore, specific surfactant proteins (SP) like SP-D are part of the innate immune system. After inhalation of various particles, they can reach the alveoli where they come into direct contact with the surfactant layer. In the present work the consequences upon interaction between surfactant and single particles are described. The influence of SP-D on allergen particle uptake by primary epithelial cells in a monoculture as well as epithelial cells, macrophages, and dendritic cells within a triple cell culture model, was investigated by flow cytometry and confocal microscopy. The secretion of inflammatory mediators was measured by Enzyme Linked Immunosorbent Assay as well as Multiplex Assay. In addition, titanium dioxide (TiO2) nanoparticles were incubated with a natural surfactant preparation. Surface tension was measured with a pulsating bubble surfactometer following particle addition and surface tension was evaluated after surface area cycling. The effects of TiO2 nanoparticles on surfactant ultrastructure were visualized by a transmission electron microscope. Incubation with SP-D led to an increase in the percentage of primary human epithelial cells which participated in particle attachment and increased secretion of the proinflammatory cytokine interleukin-8 by these cells. The number of allergen particles per cell stayed constant. In the triple cell culture model, SP-D led to an increased percentage of macrophages and epithelial cells, which participated in particle uptake. Interestingly, SP-D treatment also resulted in a trend towards decreased particle uptake per individual macrophage and dendritic cell. In addition, SP-D led to decreased secretion of interleukin-8. Addition of TiO2 nanoparticles to surfactant induced a biophysical surfactant dysfunction. This dysfunction was more pronounced after surface area cycling. In addition, ultrastructural changes of surfactant were visualized. Lamellar bodies were deformed and unilamellar vesicles were produced. The observed interactions of various particles and surfactant components could therefore play an important role in the pathophysiology of airway disease. | |||||||||||
Details der Publikation | |||||||||||
| |||||||||||