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Bovine Intestinal Alkaline Phosphatase Reduces Inflammation After Induction of Acute Myocardial Infarction in Mice
BACKGROUND: There has been increasing evidence suggesting that lipopolysaccharide or endotoxin may be an important activator of the innate immune system after acute myocardial infarction. Bovine intestinal alkaline phosphatase reduces inflammation in several endotoxin mediated diseases by dephosphor...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elmer Press
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5358284/ https://www.ncbi.nlm.nih.gov/pubmed/28357012 http://dx.doi.org/10.4021/cr81w |
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author | Fiechter, Danielle Kats, Suzanne Brands, Ruud van Middelaar, Ben Pasterkamp, Gerard de Kleijn, Dominique Seinen, Willem |
author_facet | Fiechter, Danielle Kats, Suzanne Brands, Ruud van Middelaar, Ben Pasterkamp, Gerard de Kleijn, Dominique Seinen, Willem |
author_sort | Fiechter, Danielle |
collection | PubMed |
description | BACKGROUND: There has been increasing evidence suggesting that lipopolysaccharide or endotoxin may be an important activator of the innate immune system after acute myocardial infarction. Bovine intestinal alkaline phosphatase reduces inflammation in several endotoxin mediated diseases by dephosphorylation of the lipid A moiety of lipopolysaccharide. The aim of this study was to investigate the effect of bovine intestinal alkaline phosphatase on reducing inflammation after acute myocardial infarction. METHODS: Just before permanent ligation of the left anterior descending coronary (LAD) artery to induce acute myocardial infarction in Balb/c mice, bovine intestinal alkaline phosphatase (bIAP) was administrated intravenously. After 4 hours, mice were sacrificed and the inflammatory response was assessed. Acute myocardial infarction induced the production of different cytokines, which were measured in blood. RESULTS: Treatment with bovine intestinal alkaline phosphatase resulted in a significant reduction of the pro-inflammatory cytokines IL-6, IL-1β and the chymase mouse mast cell protease-1. No difference in the production of the anti-inflammatory cytokine IL-10 was observed between the control group and the bovine intestinal alkaline phosphatase treated group. CONCLUSION: In a mouse model of permanent LAD coronary artery ligation, bIAP diminishes the pro-inflammatory responses but does not have an effect on the anti-inflammatory response in the acute phase after acute myocardial infarction. |
format | Online Article Text |
id | pubmed-5358284 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | Elmer Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-53582842017-03-29 Bovine Intestinal Alkaline Phosphatase Reduces Inflammation After Induction of Acute Myocardial Infarction in Mice Fiechter, Danielle Kats, Suzanne Brands, Ruud van Middelaar, Ben Pasterkamp, Gerard de Kleijn, Dominique Seinen, Willem Cardiol Res Original Article BACKGROUND: There has been increasing evidence suggesting that lipopolysaccharide or endotoxin may be an important activator of the innate immune system after acute myocardial infarction. Bovine intestinal alkaline phosphatase reduces inflammation in several endotoxin mediated diseases by dephosphorylation of the lipid A moiety of lipopolysaccharide. The aim of this study was to investigate the effect of bovine intestinal alkaline phosphatase on reducing inflammation after acute myocardial infarction. METHODS: Just before permanent ligation of the left anterior descending coronary (LAD) artery to induce acute myocardial infarction in Balb/c mice, bovine intestinal alkaline phosphatase (bIAP) was administrated intravenously. After 4 hours, mice were sacrificed and the inflammatory response was assessed. Acute myocardial infarction induced the production of different cytokines, which were measured in blood. RESULTS: Treatment with bovine intestinal alkaline phosphatase resulted in a significant reduction of the pro-inflammatory cytokines IL-6, IL-1β and the chymase mouse mast cell protease-1. No difference in the production of the anti-inflammatory cytokine IL-10 was observed between the control group and the bovine intestinal alkaline phosphatase treated group. CONCLUSION: In a mouse model of permanent LAD coronary artery ligation, bIAP diminishes the pro-inflammatory responses but does not have an effect on the anti-inflammatory response in the acute phase after acute myocardial infarction. Elmer Press 2011-10 2011-09-20 /pmc/articles/PMC5358284/ /pubmed/28357012 http://dx.doi.org/10.4021/cr81w Text en Copyright 2011, Fiechter et al. http://creativecommons.org/licenses/by/2.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Fiechter, Danielle Kats, Suzanne Brands, Ruud van Middelaar, Ben Pasterkamp, Gerard de Kleijn, Dominique Seinen, Willem Bovine Intestinal Alkaline Phosphatase Reduces Inflammation After Induction of Acute Myocardial Infarction in Mice |
title | Bovine Intestinal Alkaline Phosphatase Reduces Inflammation After Induction of Acute Myocardial Infarction in Mice |
title_full | Bovine Intestinal Alkaline Phosphatase Reduces Inflammation After Induction of Acute Myocardial Infarction in Mice |
title_fullStr | Bovine Intestinal Alkaline Phosphatase Reduces Inflammation After Induction of Acute Myocardial Infarction in Mice |
title_full_unstemmed | Bovine Intestinal Alkaline Phosphatase Reduces Inflammation After Induction of Acute Myocardial Infarction in Mice |
title_short | Bovine Intestinal Alkaline Phosphatase Reduces Inflammation After Induction of Acute Myocardial Infarction in Mice |
title_sort | bovine intestinal alkaline phosphatase reduces inflammation after induction of acute myocardial infarction in mice |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5358284/ https://www.ncbi.nlm.nih.gov/pubmed/28357012 http://dx.doi.org/10.4021/cr81w |
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