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Expression of von Willebrand factor, pulmonary intravascular macrophages, and Toll-like receptors in lungs of septic foals
Sepsis causes significant mortality in neonatal foals; however, there is little data describing the cellular and molecular pathways of lung inflammation in septic foals. This study was conducted to characterize lung inflammation in septic foals. Lung tissue sections from control (n = 6) and septic (...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Society of Veterinary Science
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5366298/ https://www.ncbi.nlm.nih.gov/pubmed/27297419 http://dx.doi.org/10.4142/jvs.2017.18.1.17 |
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author | Harrison, Jacqueline M. E. Quanstrom, Leah M. Robinson, Alex R. Wobeser, Bruce Anderson, Stacy L. Singh, Baljit |
author_facet | Harrison, Jacqueline M. E. Quanstrom, Leah M. Robinson, Alex R. Wobeser, Bruce Anderson, Stacy L. Singh, Baljit |
author_sort | Harrison, Jacqueline M. E. |
collection | PubMed |
description | Sepsis causes significant mortality in neonatal foals; however, there is little data describing the cellular and molecular pathways of lung inflammation in septic foals. This study was conducted to characterize lung inflammation in septic foals. Lung tissue sections from control (n = 6) and septic (n = 17) foals were compared using histology and immunohistology. Blinded pathologic scoring of hematoxylin and eosin stained samples revealed increased features of lung inflammation such as thickened alveolar septa and sequestered inflammatory cells in septic foals. Septic foal lungs showed increased expression of von Willebrand factor in blood vessels, demonstrating vascular inflammation. Use of MAC387 antibody to detect calprotectin as a reflection of mononuclear cell infiltration revealed a significant increase in their numbers in alveolar septa of lungs from septic foals compared to those from control foals. The mononuclear cells appeared to be mature macrophages and were located in the septal capillaries, suggesting they were pulmonary intravascular macrophages (PIMs). Finally, lungs from septic foals showed increased expression of Toll-like receptor 4 and 9 in mononuclear cells relative to the control. Taken together, this study is the first to show the expression of inflammatory molecules and an increase in PIMs in lungs from foals that died from sepsis. |
format | Online Article Text |
id | pubmed-5366298 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | The Korean Society of Veterinary Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-53662982017-03-28 Expression of von Willebrand factor, pulmonary intravascular macrophages, and Toll-like receptors in lungs of septic foals Harrison, Jacqueline M. E. Quanstrom, Leah M. Robinson, Alex R. Wobeser, Bruce Anderson, Stacy L. Singh, Baljit J Vet Sci Original Article Sepsis causes significant mortality in neonatal foals; however, there is little data describing the cellular and molecular pathways of lung inflammation in septic foals. This study was conducted to characterize lung inflammation in septic foals. Lung tissue sections from control (n = 6) and septic (n = 17) foals were compared using histology and immunohistology. Blinded pathologic scoring of hematoxylin and eosin stained samples revealed increased features of lung inflammation such as thickened alveolar septa and sequestered inflammatory cells in septic foals. Septic foal lungs showed increased expression of von Willebrand factor in blood vessels, demonstrating vascular inflammation. Use of MAC387 antibody to detect calprotectin as a reflection of mononuclear cell infiltration revealed a significant increase in their numbers in alveolar septa of lungs from septic foals compared to those from control foals. The mononuclear cells appeared to be mature macrophages and were located in the septal capillaries, suggesting they were pulmonary intravascular macrophages (PIMs). Finally, lungs from septic foals showed increased expression of Toll-like receptor 4 and 9 in mononuclear cells relative to the control. Taken together, this study is the first to show the expression of inflammatory molecules and an increase in PIMs in lungs from foals that died from sepsis. The Korean Society of Veterinary Science 2017-03 2017-03-21 /pmc/articles/PMC5366298/ /pubmed/27297419 http://dx.doi.org/10.4142/jvs.2017.18.1.17 Text en © 2017 The Korean Society of Veterinary Science http://creativecommons.org/licenses/by-nc/4.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Harrison, Jacqueline M. E. Quanstrom, Leah M. Robinson, Alex R. Wobeser, Bruce Anderson, Stacy L. Singh, Baljit Expression of von Willebrand factor, pulmonary intravascular macrophages, and Toll-like receptors in lungs of septic foals |
title | Expression of von Willebrand factor, pulmonary intravascular macrophages, and Toll-like receptors in lungs of septic foals |
title_full | Expression of von Willebrand factor, pulmonary intravascular macrophages, and Toll-like receptors in lungs of septic foals |
title_fullStr | Expression of von Willebrand factor, pulmonary intravascular macrophages, and Toll-like receptors in lungs of septic foals |
title_full_unstemmed | Expression of von Willebrand factor, pulmonary intravascular macrophages, and Toll-like receptors in lungs of septic foals |
title_short | Expression of von Willebrand factor, pulmonary intravascular macrophages, and Toll-like receptors in lungs of septic foals |
title_sort | expression of von willebrand factor, pulmonary intravascular macrophages, and toll-like receptors in lungs of septic foals |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5366298/ https://www.ncbi.nlm.nih.gov/pubmed/27297419 http://dx.doi.org/10.4142/jvs.2017.18.1.17 |
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