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Lipopolysaccharide regulated protein expression is only partly impaired in monocytes from patients with type I diabetes
BACKGROUND: Monocytes play an important role in innate immunity and atherosclerosis. A disturbed secretion of cytokines in lipopolysaccharide (LPS) activated monocytes from type 1 diabetes (T1D) patients has been described and may contribute to the impaired inflammatory response in these individuals...
Autores principales: | , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2006
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1524748/ https://www.ncbi.nlm.nih.gov/pubmed/16566827 http://dx.doi.org/10.1186/1475-2840-5-5 |
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author | Wehrwein, Gabriele Neumeier, Markus Schäffler, Andreas Kopp, Andrea Weigert, Johanna Abke, Sabine Schölmerich, Jürgen Buechler, Christa |
author_facet | Wehrwein, Gabriele Neumeier, Markus Schäffler, Andreas Kopp, Andrea Weigert, Johanna Abke, Sabine Schölmerich, Jürgen Buechler, Christa |
author_sort | Wehrwein, Gabriele |
collection | PubMed |
description | BACKGROUND: Monocytes play an important role in innate immunity and atherosclerosis. A disturbed secretion of cytokines in lipopolysaccharide (LPS) activated monocytes from type 1 diabetes (T1D) patients has been described and may contribute to the impaired inflammatory response in these individuals. In the present study the influence of LPS on five different proteins with a function in immunity and atherosclerosis was analyzed in monocytes from controls and T1D patients. METHODS: Monocytes were isolated from controls and T1D patients and the LPS-stimulated increase of IL-6, CXCL8, monocyte chemotactic protein 1 (CCL2, MCP-1) and superoxide dismutase (SOD 2), as well as the LPS-mediated decrease of apolipoprotein E (Apo E) in primary human monocytes from controls and T1D patients was determined. RESULTS: CCL2 and IL-6 secretion in response to LPS was found significantly reduced in monocytes from T1D patients when compared to controls whereas basal CCL2 release was similar in control and T1D cells. In contrast, CXCL8 and apolipoprotein E secretion and SOD 2 expression upon LPS stimulation is similar from T1D and control monocytes. CONCLUSION: These data indicate that LPS-mediated protein expression is only partly disturbed in monocytes from T1D patients. Reduced secretion of IL-6 and CCL2 in activated monocytes of these patients may contribute to an impaired inflammatory response and vascular disease. |
format | Text |
id | pubmed-1524748 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2006 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-15247482006-07-29 Lipopolysaccharide regulated protein expression is only partly impaired in monocytes from patients with type I diabetes Wehrwein, Gabriele Neumeier, Markus Schäffler, Andreas Kopp, Andrea Weigert, Johanna Abke, Sabine Schölmerich, Jürgen Buechler, Christa Cardiovasc Diabetol Original Investigation BACKGROUND: Monocytes play an important role in innate immunity and atherosclerosis. A disturbed secretion of cytokines in lipopolysaccharide (LPS) activated monocytes from type 1 diabetes (T1D) patients has been described and may contribute to the impaired inflammatory response in these individuals. In the present study the influence of LPS on five different proteins with a function in immunity and atherosclerosis was analyzed in monocytes from controls and T1D patients. METHODS: Monocytes were isolated from controls and T1D patients and the LPS-stimulated increase of IL-6, CXCL8, monocyte chemotactic protein 1 (CCL2, MCP-1) and superoxide dismutase (SOD 2), as well as the LPS-mediated decrease of apolipoprotein E (Apo E) in primary human monocytes from controls and T1D patients was determined. RESULTS: CCL2 and IL-6 secretion in response to LPS was found significantly reduced in monocytes from T1D patients when compared to controls whereas basal CCL2 release was similar in control and T1D cells. In contrast, CXCL8 and apolipoprotein E secretion and SOD 2 expression upon LPS stimulation is similar from T1D and control monocytes. CONCLUSION: These data indicate that LPS-mediated protein expression is only partly disturbed in monocytes from T1D patients. Reduced secretion of IL-6 and CCL2 in activated monocytes of these patients may contribute to an impaired inflammatory response and vascular disease. BioMed Central 2006-03-27 /pmc/articles/PMC1524748/ /pubmed/16566827 http://dx.doi.org/10.1186/1475-2840-5-5 Text en Copyright © 2006 Wehrwein 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 | Original Investigation Wehrwein, Gabriele Neumeier, Markus Schäffler, Andreas Kopp, Andrea Weigert, Johanna Abke, Sabine Schölmerich, Jürgen Buechler, Christa Lipopolysaccharide regulated protein expression is only partly impaired in monocytes from patients with type I diabetes |
title | Lipopolysaccharide regulated protein expression is only partly impaired in monocytes from patients with type I diabetes |
title_full | Lipopolysaccharide regulated protein expression is only partly impaired in monocytes from patients with type I diabetes |
title_fullStr | Lipopolysaccharide regulated protein expression is only partly impaired in monocytes from patients with type I diabetes |
title_full_unstemmed | Lipopolysaccharide regulated protein expression is only partly impaired in monocytes from patients with type I diabetes |
title_short | Lipopolysaccharide regulated protein expression is only partly impaired in monocytes from patients with type I diabetes |
title_sort | lipopolysaccharide regulated protein expression is only partly impaired in monocytes from patients with type i diabetes |
topic | Original Investigation |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1524748/ https://www.ncbi.nlm.nih.gov/pubmed/16566827 http://dx.doi.org/10.1186/1475-2840-5-5 |
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