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The mechanism of LPS-induced vascular endothelial cell and renal tubular cell injury in experimental disseminated intravascular coagulation (DIC)

Department of Microbiology and Immunology and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University, Aichi, Japan

Naoki Koide

Department of Microbiology and Immunology and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University, Aichi, Japan

Yutaka Kato

Department of Microbiology and Immunology and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University, Aichi, Japan

Tsuyoshi Sugiyama

Department of Microbiology and Immunology and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University, Aichi, Japan

Tomoaki Yoshida

Department of Microbiology and Immunology and Division of Bacterial Toxin, Research Center for Infectious Disease, Aichi Medical University, Aichi, Japan

The mechanism of LPS-induced tissue injury in experimental disseminated intravascular coagulation (DIC) was investigated. The generalized Shwartzman reaction (GSR) was used for an experimental murine DIC model. GSR was induced in mice by two consecutive injections of LPS. Vascular endothelial cells in various organs of those mice were stained positively by the in situ nick end labeling specific for fragmented DNA. Renal tubular cells were also stained with the nick end labeling. Fragmented nuclei were histologically detected on vascular endothelial cells and renal tubular cells in GSR-induced mice. It was suggested that apoptotic cell death might participate in development of vascular endothelial cell and renal tubular cell injury in GSR. Interferon- and ICAM-1 seemed to play an important role in the apoptosis of vascular endothelial cells. On the other hand, Fas and Fas ligand system seemed to be involved in the apoptosis of renal tubular cells. The detailed mechanism of vascular endothelial cell and renal tubular cell injury is discussed.

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