Kupffer cell inactivation prevents lipopolysaccharide-induced structural changes in the rat liver sinusoid: An electron-microscopic study |
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| Institution: | 2. Inserm U1015, Gustave Roussy, Villejuif 94800, France;3. Center for Infectious Medicine, Department of Medicine, Karolinska Institute, Huddinge 14157, Sweden;4. Inovarion, Paris 75005, France;5. Division of Immunology, Transplantation and Infectious Diseases, IRCCS San Raffaele Scientific Institute, Milan 20132, Italy;6. Vita-Salute San Raffaele University, Milan 20132, Italy;7. Shanghai Institute of Immunology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China;8. Department of Microbiology and Immunology, Immunology Translational Research Program, Yong Loo Lin School of Medicine, Immunology Program, Life Sciences Institute, National University of Singapore, Singapore 117543, Singapore;10. Biosciences and Medicine, Faculty of Health and Medical Sciences, University of Surrey, Guildford GU2 7XH, United Kingdom;12. Aix Marseille University, CNRS, INSERM, CIML, Marseille 13288, France;13. UMR INSERM U1065/UNS, C3M, Nice 06204, France;14. Centre de Recherche des Cordeliers, INSERM, Université de Paris, Sorbonne Université, IMMEDIAB Laboratory, Paris 75006, France;15. Experimental Imaging Centre, IRCCS San Raffaele Scientific Institute, Milan 20132, Italy;16. Translational Immunology Institute, SingHealth Duke-NUS Academic Medical Centre, Singapore 169856, Singapore;1. Research Service, Richard L. Roudebush VA Medical Center, Indianapolis, Indiana;2. Indiana Center for Liver Research and Division of Gastroenterology and Hepatology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana;3. Liver Unit, Department of Medicine, University of Rome Tor Vergata, Rome, Italy;4. Division of Transplant Surgery, Department of Surgery, Indiana University School of Medicine, Indianapolis, Indiana;5. Texas College of Osteopathic Medicine, The University of North Texas Health Science Center, Fort Worth, Texas;6. Research Institute, Baylor Scott & White Healthcare, Temple, Texas;7. School of Biological Sciences, Natural and Health Sciences, University of Northern Colorado, Greeley, Colorado;11. Department of Medical Physiology, Texas A&M University College of Medicine, Bryan, Texas |
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| Abstract: | Scanning and transmission electron-microscopic examination of the rat liver sinusoid was performed in this study after in vivo treatment of rats with gram-negative bacterial lipopolysaccharide (LPS, 1 mg/Kg(-1) body weight), with or without pretreatment with gadolinium chloride (GdCl3 10 mg(Kg(-1) body weight). Twenty-seven and 48 hours after GdCl3 administration, to inactivate/eliminate part of the Kupffer cell population, a decrease in the number of visualized Kupffer cells was observed, without evident effects on the sinusoidal endothelial cell or on the hepatocyte. Three and 24 hours after its administration, LPS produced ultrastructural changes in the sinusoid characterized by morphological evidence of Kupffer cell activation (i.e., swelling and expanded philopodia anchoring the Kupffer cell to the luminal surface of the sinusoidal wall), and a marked decrease in the population of endothelial cell fenestration. The reduction in the number of fenestrae was associated with a change in the diameter of fenestrae and can be interpreted as a component of the "capillarization" process of the hepatic sinusoid. Such ultrastructural changes were prevented by the administration of GdCl3 24 hours before LPS injection. Hence, these findings suggest that LPS-induced structural changes in the liver sinusoid are mediated by an LPS-induced Kupffer cell activation. Coupled with previous experimental data, showing similar effects of GdCl3 on one of the hepatic sinusoidal endothelial cell (SEC) functions, i.e., hyaluronan scavenging, the data presented in this study strongly support the view that Kupffer cells modulate both the hepatic SEC's functional as well as ultrastructural properties. (Hepatology 1996 Apr;23(4):788-96) |
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