Endogenous peroxidase activity as a marker of macrophage renewal during BCG-induced inflammation in the rat lung.

To determine whether the cytochemical localization of peroxidase activity could be used as a marker of monocyte influx into the lung during an inflammatory response, the authors studied the peroxidase phenotypes of lavaged alveolar macrophages from rats with bacille Calmette-Guérin (BCG)-induced pulmonary inflammation. Rats were immunized subcutaneously and 2 weeks later intravenously with BCG. During the early phase of pulmonary inflammation, an increase was observed in the numbers of alveolar macrophages with no peroxidase activity in the endoplasmic reticulum. These cells appeared to reflect monocyte influx into the injured lung. The later stages of inflammation were characterized by increased numbers of alveolar macrophages with peroxidase-positive endoplasmic reticulum, probably due to activation of enzymatic activity in situ. During the early phase, peroxidase activity was also observed within macrophage cytoplasmic inclusions, probably representing both primary monocyte lysosomes and internalized myeloperoxidase from inflammatory neutrophils. Serial observations indicated that the peroxidase-positive cytoplasmic inclusions became negative with time. It is concluded that inflammation-induced modulation of peroxidase activity in the endoplasmic reticulum and in cytoplasmic inclusions makes the alveolar macrophage peroxidase phenotype no more than a rough marker of monocyte influx into the inflamed lung.