Research
Lipopolysaccharide induced inflammation in the perivascular space in lungs
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* Corresponding author: Thomas Tschernig tschernig.thomas@mh-hannover.de
- † Equal contributors
1 Dept. of Functional and Applied Anatomy -4120-, Medical School of Hannover, Carl-Neuberg-Str. 1, 30625, Hannover, Germany
2 Immunology Research Group, Departments of Veterinary Biomedical Sciences and Veterinary Microbiology, Western College of Veterinary Medicine, University of Saskatchewan, 52 Campus Drive, Saskatoon, SK, S7N 5B4, Canada
3 Diagnostic Medicine and Pathobiology, 1800 Denison Avenue, Kansas State University, Manhattan, Kansas 66506, USA
Journal of Occupational Medicine and Toxicology 2008, 3:17 doi:10.1186/1745-6673-3-17
Published: 30 July 2008Abstract
Background
Lipopolysaccharide (LPS) contained in tobacco smoke and a variety of environmental and occupational dusts is a toxic agent causing lung inflammation characterized by migration of neutrophils and monocytes into alveoli. Although migration of inflammatory cells into alveoli of LPS-treated rats is well characterized, the dynamics of their accumulation in the perivascular space (PVS) leading to a perivascular inflammation (PVI) of pulmonary arteries is not well described.
Methods
Therefore, we investigated migration of neutrophils and monocytes into PVS in lungs of male Sprague-Dawley rats treated intratracheally with E. coli LPS and euthanized after 1, 6, 12, 24 and 36 hours. Control rats were treated with endotoxin-free saline. H&E stained slides were made and immunohistochemistry was performed using a monocyte marker and the chemokine Monocyte-Chemoattractant-Protein-1 (MCP-1). Computer-assisted microscopy was performed to count infiltrating cells.
Results
Surprisingly, the periarterial infiltration was not a constant finding in each animal although LPS-induced alveolitis was present. A clear tendency was observed that neutrophils were appearing in the PVS first within 6 hours after LPS application and were decreasing at later time points. In contrast, mononuclear cell infiltration was observed after 24 hours. In addition, MCP-1 expression was present in perivascular capillaries, arteries and the epithelium.
Conclusion
PVI might be a certain lung reaction pattern in the defense to infectious attacks.