ACUTE EXPERIMENTAL SILICOSIS - LUNG MORPHOLOGY, HISTOLOGY, AND MACROPHAGE CHEMOTAXIN SECRETION

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  • 1 January 1982
    • journal article
    • research article
    • Vol. 109  (1) , 27-36
Abstract
The acute inflammatory reaction in the lungs of guinea pigs produced by the intratracheal injection of silica was assessed by histologic studies and whole-lung lavage 1, 2, 4, 7 and 14 days after the intratracheal instillation of quartz particles or saline. Lavaged macrophages were cultured in vitro, and the media were assayed for chemotactic factors. This exposure to silica produced a neutrophilic inflammatory response around terminal bronchioles that was well developed within 1 day after injection. Four days after injection, neutrophils were replaced by mononuclear cells and, by 7 days, loosely organized granulomas and collagen deposition were detected in the interstitium. The number of neutrophils (PMN) recovered by lavage from experimental animals was greatest 1 day after injection and was significantly greater (P < 0.01) than that for controls at all times. The number of macrophages recovered by lavage did not exceed control levels until 7 days after injection and remained elevated thereafter. The cells recovered by lavage mirrored the changes seen in the inflamed lung. In experiments utilizing blind-well chemotactic chambers, peritoneal exudate neutrophils and macrophages migrated in greater numbers (P < 0.02) toward supernatants from cultures of alveolar macrophages lavaged from silica-exposed animals than toward supernatants from control animal macrophage cultures at each time point. Migration of normal alveolar macrophages toward supernatants from all cultures was minimal. Exposure to silica in vivo was a potent stimulus for the release of neutrophil and monocyte chemotactic factors by alveolar macrophages in vitro. The correlation between the types of inflammatory cells identified in the lung microscopically and by lavage, and the chemotactic factors released in vitro by alveolar macrophages from these lungs suggested that alveolar macrophages played a role in mediating pulmonary inflammation in this form of experimental silicosis.