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Low Glucose Concentrations Induce a Similar Inflammatory Response in Monocytes from Type 2 Diabetic Patients and Healthy Subjects
This study aims to assess the proinflammatory interleukin 1β (IL-1β) and anti-inflammatory IL-10 production by monocytes from 38 patients with type 2 diabetes and 31 controls in different glucose concentrations. Monocytes were incubated in low (2.5 mmol/L)-, normal (5.0 mmol/L)-, and high (20 mmol/L...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5684594/ https://www.ncbi.nlm.nih.gov/pubmed/29225725 http://dx.doi.org/10.1155/2017/9185272 |
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author | Piarulli, Francesco Sartore, Giovanni Sechi, Annalisa Basso, Daniela Fogar, Paola Greco, Eliana Ragazzi, Eugenio Lapolla, Annunziata |
author_facet | Piarulli, Francesco Sartore, Giovanni Sechi, Annalisa Basso, Daniela Fogar, Paola Greco, Eliana Ragazzi, Eugenio Lapolla, Annunziata |
author_sort | Piarulli, Francesco |
collection | PubMed |
description | This study aims to assess the proinflammatory interleukin 1β (IL-1β) and anti-inflammatory IL-10 production by monocytes from 38 patients with type 2 diabetes and 31 controls in different glucose concentrations. Monocytes were incubated in low (2.5 mmol/L)-, normal (5.0 mmol/L)-, and high (20 mmol/L)-glucose conditions in the presence and absence of lipopolysaccharide (LPS). Monocytes from both patients and controls only produced a significant increase in IL-1β in low-glucose conditions (p < 0.01), and this phenomenon was amplified in the presence of LPS, while it was not seen in normal- or high-glucose conditions, not even in the presence of LPS stimulation. There was no increase in IL-10 production by monocytes from either diabetic patients or controls using whatever glucose concentrations, except when treated with LPS in normal-glucose conditions. These findings seem to suggest that low-glucose conditions induce an inflammatory response in monocytes in all individuals, as an intrinsic capacity of this cell line. On the other hand, monocytes only retain their anti-inflammatory ability in response to known inflammatory stimuli such as LPS, under normal-glucose concentrations. In conclusion, human monocytes express an inflammatory pattern in low-glucose conditions in vitro. This response could contribute to explaining the higher cardiovascular risk induced by hypoglycemia in diabetic patients. |
format | Online Article Text |
id | pubmed-5684594 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-56845942017-12-10 Low Glucose Concentrations Induce a Similar Inflammatory Response in Monocytes from Type 2 Diabetic Patients and Healthy Subjects Piarulli, Francesco Sartore, Giovanni Sechi, Annalisa Basso, Daniela Fogar, Paola Greco, Eliana Ragazzi, Eugenio Lapolla, Annunziata Oxid Med Cell Longev Research Article This study aims to assess the proinflammatory interleukin 1β (IL-1β) and anti-inflammatory IL-10 production by monocytes from 38 patients with type 2 diabetes and 31 controls in different glucose concentrations. Monocytes were incubated in low (2.5 mmol/L)-, normal (5.0 mmol/L)-, and high (20 mmol/L)-glucose conditions in the presence and absence of lipopolysaccharide (LPS). Monocytes from both patients and controls only produced a significant increase in IL-1β in low-glucose conditions (p < 0.01), and this phenomenon was amplified in the presence of LPS, while it was not seen in normal- or high-glucose conditions, not even in the presence of LPS stimulation. There was no increase in IL-10 production by monocytes from either diabetic patients or controls using whatever glucose concentrations, except when treated with LPS in normal-glucose conditions. These findings seem to suggest that low-glucose conditions induce an inflammatory response in monocytes in all individuals, as an intrinsic capacity of this cell line. On the other hand, monocytes only retain their anti-inflammatory ability in response to known inflammatory stimuli such as LPS, under normal-glucose concentrations. In conclusion, human monocytes express an inflammatory pattern in low-glucose conditions in vitro. This response could contribute to explaining the higher cardiovascular risk induced by hypoglycemia in diabetic patients. Hindawi 2017 2017-10-31 /pmc/articles/PMC5684594/ /pubmed/29225725 http://dx.doi.org/10.1155/2017/9185272 Text en Copyright © 2017 Francesco Piarulli et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Piarulli, Francesco Sartore, Giovanni Sechi, Annalisa Basso, Daniela Fogar, Paola Greco, Eliana Ragazzi, Eugenio Lapolla, Annunziata Low Glucose Concentrations Induce a Similar Inflammatory Response in Monocytes from Type 2 Diabetic Patients and Healthy Subjects |
title | Low Glucose Concentrations Induce a Similar Inflammatory Response in Monocytes from Type 2 Diabetic Patients and Healthy Subjects |
title_full | Low Glucose Concentrations Induce a Similar Inflammatory Response in Monocytes from Type 2 Diabetic Patients and Healthy Subjects |
title_fullStr | Low Glucose Concentrations Induce a Similar Inflammatory Response in Monocytes from Type 2 Diabetic Patients and Healthy Subjects |
title_full_unstemmed | Low Glucose Concentrations Induce a Similar Inflammatory Response in Monocytes from Type 2 Diabetic Patients and Healthy Subjects |
title_short | Low Glucose Concentrations Induce a Similar Inflammatory Response in Monocytes from Type 2 Diabetic Patients and Healthy Subjects |
title_sort | low glucose concentrations induce a similar inflammatory response in monocytes from type 2 diabetic patients and healthy subjects |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5684594/ https://www.ncbi.nlm.nih.gov/pubmed/29225725 http://dx.doi.org/10.1155/2017/9185272 |
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