This study was designed to evaluate the role of neutrophils (PMNs) in the pathogenesis of emphysema. After administration of CdCl2 intratracheally to hamsters fed a lathyrogen, β-amino proprionitrile fumarate (BAPN), the classic lesions of emphysema developed. Administration of specific antineutrophil serum markedly reduced the PMN influx into the lungs which followed CdCl2 exposure and produced a substantial decrease in elastase and collagenase content of bronchoalveolar lavage fluid (BAL). The degree of emphysema in PMN-depleted hamsters given BAPN and CdCl2 was not different from that in hamsters given BAPN and CdCl2. Furthermore, the degree of acute lung injury following CdCl2, as determined by hydroxyproline content of BAL and by lung lipid peroxidation, was the same in PMN-depleted and non-depleted groups. Thus, PMNs were not necessary for the induction of emphysema in BAPN-CdCl2-treated hamsters. The results suggest that PMNs may not obligate mediators of emphysema.
|Original language||English (US)|
|Number of pages||8|
|Journal||American Journal of Pathology|
|State||Published - 1985|