Ozone-Induced Lamellar Body Responses in a Rat Model for Alveolar Injury and Repair

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Exposure of adult rats to 3 ppm ozone for 8 hours results in diffuse alveolar damage with well-defined sequential stages of bronchiolo-alveolar injury and repair. This model is characterized by acute pulmonary edema showing high concentration of lavage fluid protein that is maximally elevated at 24 hours with return to control level at recovery (96 hours). Using techniques that enable optimal preservation of lamellar body ultrastructure, it was demonstrated morphometrically that expansion of the vacuolated lamellar body (LB) compartment is an early, transient LB response of the type II cell to acute injury. This change appears to be initiated by increased LB secretion. The reparative stage, 24-48 hours postexposure, begins with hypertrophy rather than hyperplasia of many type II cells, resulting in a 3-fold increase of mean type II cell volume at 48 hours. During this stage there is also significant expansion of the total LB compartment with corresponding increased LB storage of surfactant disaturated phosphatidylcholine (DSPC) per type II cell. At recovery, 96 hours, the lungs contained twice the normal numbers of type II cells, but the total size of lamellar body compartment per type II cell as well as the DSPC content of the isolated lamellar body pool returned to normal levels. In contrast, accumulating surfactant DSPC in lavage fluid increased progressively throughout the reparative and recovery stages presumably due in part to parallel increase in type II cell numbers at 48 and 96 hours. Additional changes of surfactant included abnormal secretion of densely coiled lamellar bodies that accumulated in alveolar spaces at the expense of tubular myelin. These observations indicate that acute oxidant injury to alveoli initiates progressive hypertrophy followed by hyperplasia of type II cells, in association with sequential development of characteristic lamellar body changes leading to increased storage and secretion of surfactant with reduced ability to form tubular myelin.

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American Journal of Pathology, v. 132, issue 2, p. 330-340