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Lipopolysaccharide induced inflammation in the perivascular space in lungs

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...

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Autores principales: Tschernig, Thomas, Janardhan, Kyathanahalli S, Pabst, Reinhard, Singh, Baljit
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2518552/
https://www.ncbi.nlm.nih.gov/pubmed/18667067
http://dx.doi.org/10.1186/1745-6673-3-17
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author Tschernig, Thomas
Janardhan, Kyathanahalli S
Pabst, Reinhard
Singh, Baljit
author_facet Tschernig, Thomas
Janardhan, Kyathanahalli S
Pabst, Reinhard
Singh, Baljit
author_sort Tschernig, Thomas
collection PubMed
description 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.
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spelling pubmed-25185522008-08-21 Lipopolysaccharide induced inflammation in the perivascular space in lungs Tschernig, Thomas Janardhan, Kyathanahalli S Pabst, Reinhard Singh, Baljit J Occup Med Toxicol Research 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. BioMed Central 2008-07-30 /pmc/articles/PMC2518552/ /pubmed/18667067 http://dx.doi.org/10.1186/1745-6673-3-17 Text en Copyright © 2008 Tschernig et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Tschernig, Thomas
Janardhan, Kyathanahalli S
Pabst, Reinhard
Singh, Baljit
Lipopolysaccharide induced inflammation in the perivascular space in lungs
title Lipopolysaccharide induced inflammation in the perivascular space in lungs
title_full Lipopolysaccharide induced inflammation in the perivascular space in lungs
title_fullStr Lipopolysaccharide induced inflammation in the perivascular space in lungs
title_full_unstemmed Lipopolysaccharide induced inflammation in the perivascular space in lungs
title_short Lipopolysaccharide induced inflammation in the perivascular space in lungs
title_sort lipopolysaccharide induced inflammation in the perivascular space in lungs
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2518552/
https://www.ncbi.nlm.nih.gov/pubmed/18667067
http://dx.doi.org/10.1186/1745-6673-3-17
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