Abstract
ABSTRACT
Pulmonary disorders triggered by inhalation of occupational and environmental mineral particulates can be endpoints of a chronic inflammatory process in which alveolar macrophages (AMs), as a first line of defense, play a crucial role. The biological processes involved in particulate-induced activation of AMs include indirect or direct interactions of particulates with the cell membrane, subsequent stimulation of signal transduction pathways, and activation of gene transcription. Depending on the nature of particulate involved, particulate-induced activation of AMs has been shown to result in the release of potent mediators, such as reactive oxygen and nitrogen species, cytokines, eicosanoids, and growth factors. The prolonged and enhanced production of such effector molecules may result in a complex cascade of events that can contribute to the development of pulmonary disorders. This paper will give a short review of the present knowledge of AM interaction with inhaled mineral particulates and of the possible implications these interactions may have in the development of pulmonary disorders.
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