Ultrastructural study of alveolar type II cells in young rats with lipopolysaccharide-induced acute lung injury

Abstract

Objective Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are common and life-threatening disease in children with mortality as high as 40%-70%. Alveolar type Ⅱ cells (ATII cells),characterized by the presence of lamellar bodies (LBs),synthesize and secret surfactant proteins (SPs),which contribute significantly to surfactant homeostasis and pulmonary immunity.The functions of ATⅡ cells including pulmonary surfactant production are autocratically dominated by the structural integrity of ATII cells.Our study is focused on the ultrastructural alterations of AT Ⅱ cells in rats with lipopolysaccharide(LPS)-induced ALI.Methods Rat ALI models were established by intraperitoneal injection of LPS (4 mg/kg).0.9 % NS with same amount was given in the normal control group.The rats were randomly chosen and sacrificed at 24, 48 and 72 hrs after LPS injection (8 rats at each time point).Lung samples (1 mm3 of the size) were obtained from the lower parts of left lungs and fixed with 2.5% glutaraldehyde for the transmission electron microscope examination.Results The microvilli around ATII cells disappeared and the number of LBs increased at 24 hrs after LPS administration.LBs rearranged like a ring around the nuclei.It was commonly seen that two nuclei were present in one AT Ⅱ cell.Vacuole-like deformity prominently occurred in cytoplasm at 48 hrs.Giant LBs presented at the same time.The shapes of nuclei were irregular and some of the borders were unclear at 48 and 72 hrs.The remnant of ruptured LBs scattered in cytoplasm at 72 hrs.The number of LBs reduced obviously.Karyolysis occurred in some of the nuclei.Conclusions The ALI-related alterations of ATII cells characterized by the changes of LBs,nuclei,and nucleoli were time-dependent. ATII cell injury was serious at 48 and 72 hrs.This may lead to the insufficiency of pulmonary surfactant synthesis and unstability of pulmonary homeostasis,which contributed to to the pathogenesis of acute lung injury. Key words: Lipopolysaccharide; Acute lung injury; Alveolar typeⅡcells; Surfacant prote