The ability of long amosite asbestos fibers (LFA), vitreous fibers (MMVF 21 and CODE 100/475), and ceramic fibers (silicon carbide and RCF 1) to stimulate superoxide production in isolated rat alveolar macrophages is examined. The cells were exposed to both naked fibers (uncoated) and fibers coated with rat immunoglobulin (IgG), a normal component of lung lining fluid. The affinity for IgG of the various fibers was assessed by quantifying the binding of 125I-labeled IgG onto the fiber surface. Naked fibers stimulated a modest release of superoxide anion from alveolar macrophages, which was not obviously dose dependent. When IgG was adsorbed onto fibers of MMVF 21 and RCF 1, there was a dramatic increase in superoxide release, which correlated well with their high affinity for IgG.IgG-adsorbed code 100/475 and silicon carbide whiskers (SiCW) stimulated only modest superoxide release, and the fibers showed a correspondingly poor affinity for the opsonin. Conversely, the adsorbed fibers of LFA, generated a dramatic increase in superoxide release from the macrophages, despite a relatively poor adsorption of IgG. This study demonstrates the potential for components of the lung lining fluid to modify the response of alveolar macrophages to respirable natural and man-made fibers. It also draws attention to fiber-specific differences in adsorptive capacity and subsequent biological activity between these fiber types in vitro and, by implication, in vivo.
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Hill et al. (1996) studied this question.
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