Type 2 diabetes mellitus is associated with impaired cytokine response and adhesion molecule expression in human endotoxemia
Purpose Type 2 diabetes is associated with an increased risk of acquiring infectious diseases and developing sepsis. This may partly be due to immune dysfunction. We investigated the in vivo innate immune response of type 2 diabetic persons to an intravenous injection of E. coli lipopolysaccharide (...
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Veröffentlicht in: | Intensive care medicine 2010-09, Vol.36 (9), p.1548-1555 |
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description | Purpose
Type 2 diabetes is associated with an increased risk of acquiring infectious diseases and developing sepsis. This may partly be due to immune dysfunction. We investigated the in vivo innate immune response of type 2 diabetic persons to an intravenous injection of
E. coli
lipopolysaccharide (LPS).
Methods
After ethics approval, informed consent and a thorough physical examination, 19 type 2 diabetic patients and 23 healthy controls were included. LPS was given as an intravenous bolus injection of 0.3 ng/kg. Physiological variables, white blood cell count, and plasma concentrations of tumour necrosis factor (TNF), interleukin-6 (IL-6), interleukin-1 receptor antagonist (IL-1ra), and the adhesion molecules E-selectin, vascular adhesion molecule (VCAM)-1, and intracellular adhesion molecule (ICAM)-1 were measured hourly for 8 h.
Results
LPS injection induced a systemic inflammatory response with increases in neutrophils, temperature, heart rate and plasma concentrations of cytokines and adhesion molecules in healthy and type 2 diabetic volunteers. Type 2 diabetes was associated with less pronounced LPS-induced increases in TNF, IL-1ra, VCAM-1 and ICAM-1. There was a trend towards an attenuated upregulation of E-selectin in diabetics, even though the plasma concentration tended to be generally higher compared to healthy controls.
Conclusions
Patients with type 2 diabetes exhibit an attenuated increase in plasma levels of TNF and IL-1ra, as well as an attenuated upregulation of VCAM-1 and ICAM-1 to LPS in vivo. This finding may provide a mechanistic explanation for the adverse outcome seen during infectious diseases in diabetic patients. |
doi_str_mv | 10.1007/s00134-010-1845-1 |
format | Article |
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Type 2 diabetes is associated with an increased risk of acquiring infectious diseases and developing sepsis. This may partly be due to immune dysfunction. We investigated the in vivo innate immune response of type 2 diabetic persons to an intravenous injection of
E. coli
lipopolysaccharide (LPS).
Methods
After ethics approval, informed consent and a thorough physical examination, 19 type 2 diabetic patients and 23 healthy controls were included. LPS was given as an intravenous bolus injection of 0.3 ng/kg. Physiological variables, white blood cell count, and plasma concentrations of tumour necrosis factor (TNF), interleukin-6 (IL-6), interleukin-1 receptor antagonist (IL-1ra), and the adhesion molecules E-selectin, vascular adhesion molecule (VCAM)-1, and intracellular adhesion molecule (ICAM)-1 were measured hourly for 8 h.
Results
LPS injection induced a systemic inflammatory response with increases in neutrophils, temperature, heart rate and plasma concentrations of cytokines and adhesion molecules in healthy and type 2 diabetic volunteers. Type 2 diabetes was associated with less pronounced LPS-induced increases in TNF, IL-1ra, VCAM-1 and ICAM-1. There was a trend towards an attenuated upregulation of E-selectin in diabetics, even though the plasma concentration tended to be generally higher compared to healthy controls.
Conclusions
Patients with type 2 diabetes exhibit an attenuated increase in plasma levels of TNF and IL-1ra, as well as an attenuated upregulation of VCAM-1 and ICAM-1 to LPS in vivo. This finding may provide a mechanistic explanation for the adverse outcome seen during infectious diseases in diabetic patients.</description><identifier>ISSN: 0342-4642</identifier><identifier>EISSN: 1432-1238</identifier><identifier>DOI: 10.1007/s00134-010-1845-1</identifier><identifier>PMID: 20229041</identifier><identifier>CODEN: ICMED9</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Adaptive Immunity - immunology ; Adult ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Anesthesiology ; Associated diseases and complications ; Biological and medical sciences ; Biomarkers - blood ; Blood cell count ; Cell Adhesion Molecules - metabolism ; Communicable diseases ; Critical Care Medicine ; Cytokines - blood ; Development and progression ; Diabetes Mellitus, Type 2 - immunology ; Diabetes. Impaired glucose tolerance ; Diabetics ; Emergency Medicine ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Endotoxemia - metabolism ; Endotoxins - pharmacology ; Escherichia coli ; Ethical aspects ; Ethylenediaminetetraacetic acid ; Heart beat ; Humans ; Immune response ; Infection ; Intensive ; Intensive care medicine ; Interleukin-1 - blood ; Interleukins ; Lipopolysaccharides - pharmacology ; Male ; Medical sciences ; Medicine ; Medicine & Public Health ; Middle Aged ; Original ; Pain Medicine ; Pediatrics ; Physiological aspects ; Pneumology/Respiratory System ; Tumor necrosis factor ; Tumor Necrosis Factor-alpha - analysis ; Type 2 diabetes ; Vascular Cell Adhesion Molecule-1 - blood</subject><ispartof>Intensive care medicine, 2010-09, Vol.36 (9), p.1548-1555</ispartof><rights>Copyright jointly held by Springer and ESICM 2010</rights><rights>2015 INIST-CNRS</rights><rights>COPYRIGHT 2010 Springer</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c537t-3d3a86eb3063816ca83dab0a4cbd048d007088fce1f5e89844684f0d3fbd35be3</citedby><cites>FETCH-LOGICAL-c537t-3d3a86eb3063816ca83dab0a4cbd048d007088fce1f5e89844684f0d3fbd35be3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00134-010-1845-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00134-010-1845-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51298</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23170489$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20229041$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Andreasen, Anne Sofie</creatorcontrib><creatorcontrib>Pedersen-Skovsgaard, Theis</creatorcontrib><creatorcontrib>Berg, Ronan M. G.</creatorcontrib><creatorcontrib>Svendsen, Kira Dynnes</creatorcontrib><creatorcontrib>Feldt-Rasmussen, Bo</creatorcontrib><creatorcontrib>Pedersen, Bente K.</creatorcontrib><creatorcontrib>Møller, Kirsten</creatorcontrib><title>Type 2 diabetes mellitus is associated with impaired cytokine response and adhesion molecule expression in human endotoxemia</title><title>Intensive care medicine</title><addtitle>Intensive Care Med</addtitle><addtitle>Intensive Care Med</addtitle><description>Purpose
Type 2 diabetes is associated with an increased risk of acquiring infectious diseases and developing sepsis. This may partly be due to immune dysfunction. We investigated the in vivo innate immune response of type 2 diabetic persons to an intravenous injection of
E. coli
lipopolysaccharide (LPS).
Methods
After ethics approval, informed consent and a thorough physical examination, 19 type 2 diabetic patients and 23 healthy controls were included. LPS was given as an intravenous bolus injection of 0.3 ng/kg. Physiological variables, white blood cell count, and plasma concentrations of tumour necrosis factor (TNF), interleukin-6 (IL-6), interleukin-1 receptor antagonist (IL-1ra), and the adhesion molecules E-selectin, vascular adhesion molecule (VCAM)-1, and intracellular adhesion molecule (ICAM)-1 were measured hourly for 8 h.
Results
LPS injection induced a systemic inflammatory response with increases in neutrophils, temperature, heart rate and plasma concentrations of cytokines and adhesion molecules in healthy and type 2 diabetic volunteers. Type 2 diabetes was associated with less pronounced LPS-induced increases in TNF, IL-1ra, VCAM-1 and ICAM-1. There was a trend towards an attenuated upregulation of E-selectin in diabetics, even though the plasma concentration tended to be generally higher compared to healthy controls.
Conclusions
Patients with type 2 diabetes exhibit an attenuated increase in plasma levels of TNF and IL-1ra, as well as an attenuated upregulation of VCAM-1 and ICAM-1 to LPS in vivo. This finding may provide a mechanistic explanation for the adverse outcome seen during infectious diseases in diabetic patients.</description><subject>Adaptive Immunity - immunology</subject><subject>Adult</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Anesthesiology</subject><subject>Associated diseases and complications</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - blood</subject><subject>Blood cell count</subject><subject>Cell Adhesion Molecules - metabolism</subject><subject>Communicable diseases</subject><subject>Critical Care Medicine</subject><subject>Cytokines - blood</subject><subject>Development and progression</subject><subject>Diabetes Mellitus, Type 2 - immunology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Diabetics</subject><subject>Emergency Medicine</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Endotoxemia - metabolism</subject><subject>Endotoxins - pharmacology</subject><subject>Escherichia coli</subject><subject>Ethical aspects</subject><subject>Ethylenediaminetetraacetic acid</subject><subject>Heart beat</subject><subject>Humans</subject><subject>Immune response</subject><subject>Infection</subject><subject>Intensive</subject><subject>Intensive care medicine</subject><subject>Interleukin-1 - blood</subject><subject>Interleukins</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Original</subject><subject>Pain Medicine</subject><subject>Pediatrics</subject><subject>Physiological aspects</subject><subject>Pneumology/Respiratory System</subject><subject>Tumor necrosis factor</subject><subject>Tumor Necrosis Factor-alpha - analysis</subject><subject>Type 2 diabetes</subject><subject>Vascular Cell Adhesion Molecule-1 - blood</subject><issn>0342-4642</issn><issn>1432-1238</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkt9rFDEQxxdR7Fn9A3yRoIhPW_Nrd3OPpbQqFHypz2E2mb1L3U3WZBd74B9vrntalBNJIMzk850wk29RvGT0jFHavE-UMiFLymjJlKxK9qhYMSl4ybhQj4sVFZKXspb8pHiW0m2mm7piT4sTTjlfU8lWxY-b3YiEE-ugxQkTGbDv3TQn4hKBlIJxMKEl3920JW4YwcUcmd0UvjqPJGIag09IwFsCdovJBU-G0KOZeyR4N2biPuc82c4DeILehinc4eDgefGkgz7hi8N5Wny5ury5-Fhef_7w6eL8ujSVaKZSWAGqxlbQWihWG1DCQktBmtZSqWweBVWqM8i6CtVaSVkr2VErutaKqkVxWrxb6o4xfJsxTXpwyeRGwWOYk25qzhXlSv6flGotFVuLTL7-i7wNc_S5jQzVUom8M_RmgTbQo3a-C1MEsy-pzxuef0rV96XKI9QGPUbog8fO5fQf_NkRPi-bh2qOCtgiMDGkFLHTY3QDxJ1mVO-dpBcnabqPs5M0y5pXh_7mdkD7W_HLOhl4ewAgGei7CN649MAJ1uTPWWeOL1zKV36D8WFQ_379JzUA35U</recordid><startdate>20100901</startdate><enddate>20100901</enddate><creator>Andreasen, Anne Sofie</creator><creator>Pedersen-Skovsgaard, Theis</creator><creator>Berg, Ronan M. G.</creator><creator>Svendsen, Kira Dynnes</creator><creator>Feldt-Rasmussen, Bo</creator><creator>Pedersen, Bente K.</creator><creator>Møller, Kirsten</creator><general>Springer-Verlag</general><general>Springer</general><general>Springer Nature B.V</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7Z</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7T5</scope><scope>7U1</scope><scope>7U2</scope><scope>C1K</scope><scope>H94</scope></search><sort><creationdate>20100901</creationdate><title>Type 2 diabetes mellitus is associated with impaired cytokine response and adhesion molecule expression in human endotoxemia</title><author>Andreasen, Anne Sofie ; Pedersen-Skovsgaard, Theis ; Berg, Ronan M. G. ; Svendsen, Kira Dynnes ; Feldt-Rasmussen, Bo ; Pedersen, Bente K. ; Møller, Kirsten</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c537t-3d3a86eb3063816ca83dab0a4cbd048d007088fce1f5e89844684f0d3fbd35be3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adaptive Immunity - immunology</topic><topic>Adult</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Anesthesiology</topic><topic>Associated diseases and complications</topic><topic>Biological and medical sciences</topic><topic>Biomarkers - blood</topic><topic>Blood cell count</topic><topic>Cell Adhesion Molecules - metabolism</topic><topic>Communicable diseases</topic><topic>Critical Care Medicine</topic><topic>Cytokines - blood</topic><topic>Development and progression</topic><topic>Diabetes Mellitus, Type 2 - immunology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Diabetics</topic><topic>Emergency Medicine</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Endotoxemia - metabolism</topic><topic>Endotoxins - pharmacology</topic><topic>Escherichia coli</topic><topic>Ethical aspects</topic><topic>Ethylenediaminetetraacetic acid</topic><topic>Heart beat</topic><topic>Humans</topic><topic>Immune response</topic><topic>Infection</topic><topic>Intensive</topic><topic>Intensive care medicine</topic><topic>Interleukin-1 - blood</topic><topic>Interleukins</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Original</topic><topic>Pain Medicine</topic><topic>Pediatrics</topic><topic>Physiological aspects</topic><topic>Pneumology/Respiratory System</topic><topic>Tumor necrosis factor</topic><topic>Tumor Necrosis Factor-alpha - analysis</topic><topic>Type 2 diabetes</topic><topic>Vascular Cell Adhesion Molecule-1 - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Andreasen, Anne Sofie</creatorcontrib><creatorcontrib>Pedersen-Skovsgaard, Theis</creatorcontrib><creatorcontrib>Berg, Ronan M. G.</creatorcontrib><creatorcontrib>Svendsen, Kira Dynnes</creatorcontrib><creatorcontrib>Feldt-Rasmussen, Bo</creatorcontrib><creatorcontrib>Pedersen, Bente K.</creatorcontrib><creatorcontrib>Møller, Kirsten</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biochemistry Abstracts 1</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>Risk Abstracts</collection><collection>Safety Science and Risk</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Intensive care medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Andreasen, Anne Sofie</au><au>Pedersen-Skovsgaard, Theis</au><au>Berg, Ronan M. G.</au><au>Svendsen, Kira Dynnes</au><au>Feldt-Rasmussen, Bo</au><au>Pedersen, Bente K.</au><au>Møller, Kirsten</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Type 2 diabetes mellitus is associated with impaired cytokine response and adhesion molecule expression in human endotoxemia</atitle><jtitle>Intensive care medicine</jtitle><stitle>Intensive Care Med</stitle><addtitle>Intensive Care Med</addtitle><date>2010-09-01</date><risdate>2010</risdate><volume>36</volume><issue>9</issue><spage>1548</spage><epage>1555</epage><pages>1548-1555</pages><issn>0342-4642</issn><eissn>1432-1238</eissn><coden>ICMED9</coden><abstract>Purpose
Type 2 diabetes is associated with an increased risk of acquiring infectious diseases and developing sepsis. This may partly be due to immune dysfunction. We investigated the in vivo innate immune response of type 2 diabetic persons to an intravenous injection of
E. coli
lipopolysaccharide (LPS).
Methods
After ethics approval, informed consent and a thorough physical examination, 19 type 2 diabetic patients and 23 healthy controls were included. LPS was given as an intravenous bolus injection of 0.3 ng/kg. Physiological variables, white blood cell count, and plasma concentrations of tumour necrosis factor (TNF), interleukin-6 (IL-6), interleukin-1 receptor antagonist (IL-1ra), and the adhesion molecules E-selectin, vascular adhesion molecule (VCAM)-1, and intracellular adhesion molecule (ICAM)-1 were measured hourly for 8 h.
Results
LPS injection induced a systemic inflammatory response with increases in neutrophils, temperature, heart rate and plasma concentrations of cytokines and adhesion molecules in healthy and type 2 diabetic volunteers. Type 2 diabetes was associated with less pronounced LPS-induced increases in TNF, IL-1ra, VCAM-1 and ICAM-1. There was a trend towards an attenuated upregulation of E-selectin in diabetics, even though the plasma concentration tended to be generally higher compared to healthy controls.
Conclusions
Patients with type 2 diabetes exhibit an attenuated increase in plasma levels of TNF and IL-1ra, as well as an attenuated upregulation of VCAM-1 and ICAM-1 to LPS in vivo. This finding may provide a mechanistic explanation for the adverse outcome seen during infectious diseases in diabetic patients.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>20229041</pmid><doi>10.1007/s00134-010-1845-1</doi><tpages>8</tpages></addata></record> |
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source | MEDLINE; Springer Nature - Complete Springer Journals |
subjects | Adaptive Immunity - immunology Adult Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Anesthesiology Associated diseases and complications Biological and medical sciences Biomarkers - blood Blood cell count Cell Adhesion Molecules - metabolism Communicable diseases Critical Care Medicine Cytokines - blood Development and progression Diabetes Mellitus, Type 2 - immunology Diabetes. Impaired glucose tolerance Diabetics Emergency Medicine Endocrine pancreas. Apud cells (diseases) Endocrinopathies Endotoxemia - metabolism Endotoxins - pharmacology Escherichia coli Ethical aspects Ethylenediaminetetraacetic acid Heart beat Humans Immune response Infection Intensive Intensive care medicine Interleukin-1 - blood Interleukins Lipopolysaccharides - pharmacology Male Medical sciences Medicine Medicine & Public Health Middle Aged Original Pain Medicine Pediatrics Physiological aspects Pneumology/Respiratory System Tumor necrosis factor Tumor Necrosis Factor-alpha - analysis Type 2 diabetes Vascular Cell Adhesion Molecule-1 - blood |
title | Type 2 diabetes mellitus is associated with impaired cytokine response and adhesion molecule expression in human endotoxemia |
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