Response of normal and beige mouse alveolar type 2 cells to lung injury.
To study the relation between normal and abnormal alveolar type 2 cells and lung repair after injury, and to gain insight into the defect responsible for the giant lamellar bodies in type 2 cells of the beige mouse (an animal model of the Chediak-Higashi syndrome), we produced lung injury with a single injection of butylated hydroxytoluene (BHT). Type 2 cell proliferation and differentiation were analyzed in light microscopic autoradiographs of mice that had received tritiated thymidine (3H-T) at intervals after the injection of BHT. The approximate age of 3H-T labeled type 2 cells and lamellar body volume density and area were correlated by combining light microscopic autoradiography with ultrastructural morphometry. Type 2 cell proliferation and differentiation were identical in normal and in beige mice. In normal mice, the lamellar body area per cell was unchanged at the time periods studied. In beige mice, the lamellar body area per cell, which was initially 9 times that of the normal mice, decreased to nearly normal values after mitosis, and then increased over the subsequent 7 days of study. Thus, the abnormal type 2 cell of the beige mouse was able to proliferate and differentiate in a normal fashion after lung injury. The beige mouse defect, which results in impaired lamellar body release, was transiently corrected in the perimitotic period. The postmitotic enlargement of lamellar bodies provided a model for studying the basic defect in the Chediak-Higashi syndrome and the process of type 2 cell maturation.
D000818:Animals; D002454:Cell Differentiation; D002455:Cell Division; D002609:Chediak-Higashi Syndrome / Q000235:genetics*; D005260:Female; D008168:Lung / Q000648:ultrastructure; D055370:Lung Injury; D051379:Mice; D008817:Mice, Mutant Strains / Q000502:physiology*; D008854:Microscopy, Electron; D011650:Pulmonary Alveoli / Q000648:ultrastructure*; D014945:Wound Healing