Engineered carbon nanoparticles alter macrophage immune function and initiate airway hyper-responsiveness in the BALB/c mouse model

With the mass production of fullerenes currently underway, and the mass production of carbon nanotubes soon to follow, only a few studies have examined the biological consequences of manmade nanoparticle exposure in the mammalian system. This study examines carbon nanoparticle (CNP) exposure in both in vitro (murine BALB/c alveolar macrophages) and in vivo (murine BALB/c intranasal instillations) systems. Three types of CNP were examined (single-walled nanotubes, multi-walled nanotubes, and C60 fullerenes). In vitro macrophage experiments included measurements of morphology changes, apoptosis, viability, and antigen-presenting cell function in response to CNP exposure. In vivo mouse experiments determined the inflammatory potential of CNP exposure in the lung using a BUXCO™ apparatus along with cell differentials and cell morphology. This study presents evidence that CNP, accumulated in the plasma membranes of cells (disrupting lipid rafts), increased alveolar macrophage function with regard to antigen-presentation, significantly exacerbated airway hyper-responsiveness, and caused an influx of macrophages into the lung by posited mechanisms that involve the unique molecular and physical properties of CNP.