Infection-induced inflammatory response of adipocytes in vitro
Background: Abdominal obesity plays an important role in the development of insulin resistance, diabetes mellitus and atherosclerosis. The exact pathophysiological mechanisms are unclear but adipocyte dysfunction is thought to be crucial. Infections are associated with the development of atheroscler...
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| Vydané v: | International Journal of Obesity Ročník 32; číslo 6; s. 892 - 901 |
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| Hlavní autori: | , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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London
Nature Publishing Group UK
01.06.2008
Nature Publishing Nature Publishing Group |
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| ISSN: | 0307-0565, 1476-5497, 1476-5497 |
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| Abstract | Background: Abdominal obesity plays an important role in the development of insulin resistance, diabetes mellitus and atherosclerosis. The exact pathophysiological mechanisms are unclear but adipocyte dysfunction is thought to be crucial. Infections are associated with the development of atherosclerosis as well as diabetes. In this study we investigated whether adipocytes can be infected and whether this results in production of inflammatory cytokines relevant for the development of atherosclerosis and diabetes. Methods: Pre-adipocytes were cultured and differentiated into mature adipocytes in vitro. Adipocytes and pre-adipocytes were incubated with infective and heat-inactivated Chlamydia pneumoniae, cytomegalovirus (CMV), adenovirus (Ad) subtypes 2 and 36, influenza A and respiratory syncitial virus (RSV). After 48 h, adiponectin, interleukin-6 (IL-6), tumor necrosis factor- (TNF-) and plasminogen activator inhibitor-1 (PAI-1) were measured in supernatants. Results: Infection of adipocytes with Ad-36, CMV and RSV resulted in increased IL-6 production from 19222 pg ml- 1 (uninfected) to 103086 pg ml- 1, 83859 pg ml- 1 and 1241191 pg ml- 1, respectively (all P<0.01 vs control). In addition, Ad-36 infection slightly reduced PAI production in adipocytes (28526.8 ng ml- 1 vs uninfected: 47771.2 ng ml- 1; P=0.05) and pre-adipocytes (70943.3 ng ml- 1 vs uninfected: 107171.8 ng ml- 1; P<0.01). In contrast, human Ad type 2 did not exert any effect on IL-6 or PAI production. None of the microorganisms induced significant changes in adiponectin and/or TNF- production. Conclusions: Adipocytes can be infected with several microorganisms in vitro. Infection of adipocytes with Ad-36, but not Ad-2 leads to increased production of IL-6 which might contribute to chronic low-grade inflammation, a process known to be involved in the development of cardiovascular diseases and type 2 diabetes. |
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| AbstractList | Background: Abdominal obesity plays an important role in the development of insulin resistance, diabetes mellitus and atherosclerosis. The exact pathophysiological mechanisms are unclear but adipocyte dysfunction is thought to be crucial. Infections are associated with the development of atherosclerosis as well as diabetes. In this study we investigated whether adipocytes can be infected and whether this results in production of inflammatory cytokines relevant for the development of atherosclerosis and diabetes. Methods: Pre-adipocytes were cultured and differentiated into mature adipocytes in vitro. Adipocytes and pre-adipocytes were incubated with infective and heat-inactivated Chlamydia pneumoniae, cytomegalovirus (CMV), adenovirus (Ad) subtypes 2 and 36, influenza A and respiratory syncitial virus (RSV). After 48 h, adiponectin, interleukin-6 (IL-6), tumor necrosis factor- alpha (TNF- alpha ) and plasminogen activator inhibitor-1 (PAI-1) were measured in supernatants. Results: Infection of adipocytes with Ad-36, CMV and RSV resulted in increased IL-6 production from 192 plus or minus 22 pg ml super(-1) (uninfected) to 1030 plus or minus 86 pg ml super(-1), 838 plus or minus 59 pg ml super(-1) and 1241 plus or minus 191 pg ml super(-1), respectively (all P<0.01 vs control). In addition, Ad-36 infection slightly reduced PAI production in adipocytes (285 plus or minus 26.8 ng ml super(-1) vs uninfected: 477 plus or minus 71.2 ng ml super(-1); P = 0.05) and pre-adipocytes (709 plus or minus 43.3 ng ml super(-1) vs uninfected: 1071 plus or minus 71.8 ng ml super(-1); P<0.01). In contrast, human Ad type 2 did not exert any effect on IL-6 or PAI production. None of the microorganisms induced significant changes in adiponectin and/or TNF- alpha production. Conclusions: Adipocytes can be infected with several microorganisms in vitro. Infection of adipocytes with Ad-36, but not Ad-2 leads to increased production of IL-6 which might contribute to chronic low-grade inflammation, a process known to be involved in the development of cardiovascular diseases and type 2 diabetes. Background: Abdominal obesity plays an important role in the development of insulin resistance, diabetes mellitus and atherosclerosis. The exact pathophysiological mechanisms are unclear but adipocyte dysfunction is thought to be crucial. Infections are associated with the development of atherosclerosis as well as diabetes. In this study we investigated whether adipocytes can be infected and whether this results in production of inflammatory cytokines relevant for the development of atherosclerosis and diabetes. Methods: Pre-adipocytes were cultured and differentiated into mature adipocytes in vitro. Adipocytes and pre-adipocytes were incubated with infective and heat-inactivated Chlamydia pneumoniae, cytomegalovirus (CMV), adenovirus (Ad) subtypes 2 and 36, influenza A and respiratory syncitial virus (RSV). After 48 h, adiponectin, interleukin-6 (IL-6), tumor necrosis factor- (TNF-) and plasminogen activator inhibitor-1 (PAI-1) were measured in supernatants. Results: Infection of adipocytes with Ad-36, CMV and RSV resulted in increased IL-6 production from 19222 pg ml- 1 (uninfected) to 103086 pg ml- 1, 83859 pg ml- 1 and 1241191 pg ml- 1, respectively (all P<0.01 vs control). In addition, Ad-36 infection slightly reduced PAI production in adipocytes (28526.8 ng ml- 1 vs uninfected: 47771.2 ng ml- 1; P=0.05) and pre-adipocytes (70943.3 ng ml- 1 vs uninfected: 107171.8 ng ml- 1; P<0.01). In contrast, human Ad type 2 did not exert any effect on IL-6 or PAI production. None of the microorganisms induced significant changes in adiponectin and/or TNF- production. Conclusions: Adipocytes can be infected with several microorganisms in vitro. Infection of adipocytes with Ad-36, but not Ad-2 leads to increased production of IL-6 which might contribute to chronic low-grade inflammation, a process known to be involved in the development of cardiovascular diseases and type 2 diabetes. Abdominal obesity plays an important role in the development of insulin resistance, diabetes mellitus and atherosclerosis. The exact pathophysiological mechanisms are unclear but adipocyte dysfunction is thought to be crucial. Infections are associated with the development of atherosclerosis as well as diabetes. In this study we investigated whether adipocytes can be infected and whether this results in production of inflammatory cytokines relevant for the development of atherosclerosis and diabetes.BACKGROUNDAbdominal obesity plays an important role in the development of insulin resistance, diabetes mellitus and atherosclerosis. The exact pathophysiological mechanisms are unclear but adipocyte dysfunction is thought to be crucial. Infections are associated with the development of atherosclerosis as well as diabetes. In this study we investigated whether adipocytes can be infected and whether this results in production of inflammatory cytokines relevant for the development of atherosclerosis and diabetes.Pre-adipocytes were cultured and differentiated into mature adipocytes in vitro. Adipocytes and pre-adipocytes were incubated with infective and heat-inactivated Chlamydia pneumoniae, cytomegalovirus (CMV), adenovirus (Ad) subtypes 2 and 36, influenza A and respiratory syncitial virus (RSV). After 48 h, adiponectin, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) and plasminogen activator inhibitor-1 (PAI-1) were measured in supernatants.METHODSPre-adipocytes were cultured and differentiated into mature adipocytes in vitro. Adipocytes and pre-adipocytes were incubated with infective and heat-inactivated Chlamydia pneumoniae, cytomegalovirus (CMV), adenovirus (Ad) subtypes 2 and 36, influenza A and respiratory syncitial virus (RSV). After 48 h, adiponectin, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) and plasminogen activator inhibitor-1 (PAI-1) were measured in supernatants.Infection of adipocytes with Ad-36, CMV and RSV resulted in increased IL-6 production from 192+/-22 pg ml(-1) (uninfected) to 1030+/-86 pg ml(-1), 838+/-59 pg ml(-1) and 1241+/-191 pg ml(-1), respectively (all P<0.01 vs control). In addition, Ad-36 infection slightly reduced PAI production in adipocytes (285+/-26.8 ng ml(-1) vs uninfected: 477+/-71.2 ng ml(-1); P=0.05) and pre-adipocytes (709+/-43.3 ng ml(-1) vs uninfected: 1071+/-71.8 ng ml(-1); P<0.01). In contrast, human Ad type 2 did not exert any effect on IL-6 or PAI production. None of the microorganisms induced significant changes in adiponectin and/or TNF-alpha production.RESULTSInfection of adipocytes with Ad-36, CMV and RSV resulted in increased IL-6 production from 192+/-22 pg ml(-1) (uninfected) to 1030+/-86 pg ml(-1), 838+/-59 pg ml(-1) and 1241+/-191 pg ml(-1), respectively (all P<0.01 vs control). In addition, Ad-36 infection slightly reduced PAI production in adipocytes (285+/-26.8 ng ml(-1) vs uninfected: 477+/-71.2 ng ml(-1); P=0.05) and pre-adipocytes (709+/-43.3 ng ml(-1) vs uninfected: 1071+/-71.8 ng ml(-1); P<0.01). In contrast, human Ad type 2 did not exert any effect on IL-6 or PAI production. None of the microorganisms induced significant changes in adiponectin and/or TNF-alpha production.Adipocytes can be infected with several microorganisms in vitro. Infection of adipocytes with Ad-36, but not Ad-2 leads to increased production of IL-6 which might contribute to chronic low-grade inflammation, a process known to be involved in the development of cardiovascular diseases and type 2 diabetes.CONCLUSIONSAdipocytes can be infected with several microorganisms in vitro. Infection of adipocytes with Ad-36, but not Ad-2 leads to increased production of IL-6 which might contribute to chronic low-grade inflammation, a process known to be involved in the development of cardiovascular diseases and type 2 diabetes. Abdominal obesity plays an important role in the development of insulin resistance, diabetes mellitus and atherosclerosis. The exact pathophysiological mechanisms are unclear but adipocyte dysfunction is thought to be crucial. Infections are associated with the development of atherosclerosis as well as diabetes. In this study we investigated whether adipocytes can be infected and whether this results in production of inflammatory cytokines relevant for the development of atherosclerosis and diabetes. Pre-adipocytes were cultured and differentiated into mature adipocytes in vitro. Adipocytes and pre-adipocytes were incubated with infective and heat-inactivated Chlamydia pneumoniae, cytomegalovirus (CMV), adenovirus (Ad) subtypes 2 and 36, influenza A and respiratory syncitial virus (RSV). After 48 h, adiponectin, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) and plasminogen activator inhibitor-1 (PAI-1) were measured in supernatants. Infection of adipocytes with Ad-36, CMV and RSV resulted in increased IL-6 production from 192+/-22 pg ml(-1) (uninfected) to 1030+/-86 pg ml(-1), 838+/-59 pg ml(-1) and 1241+/-191 pg ml(-1), respectively (all P<0.01 vs control). In addition, Ad-36 infection slightly reduced PAI production in adipocytes (285+/-26.8 ng ml(-1) vs uninfected: 477+/-71.2 ng ml(-1); P=0.05) and pre-adipocytes (709+/-43.3 ng ml(-1) vs uninfected: 1071+/-71.8 ng ml(-1); P<0.01). In contrast, human Ad type 2 did not exert any effect on IL-6 or PAI production. None of the microorganisms induced significant changes in adiponectin and/or TNF-alpha production. Adipocytes can be infected with several microorganisms in vitro. Infection of adipocytes with Ad-36, but not Ad-2 leads to increased production of IL-6 which might contribute to chronic low-grade inflammation, a process known to be involved in the development of cardiovascular diseases and type 2 diabetes. Abdominal obesity plays an important role in the development of insulin resistance, diabetes mellitus and atherosclerosis. The exact pathophysiological mechanisms are unclear but adipocyte dysfunction is thought to be crucial. Infections are associated with the development of atherosclerosis as well as diabetes. In this study we investigated whether adipocytes can be infected and whether this results in production of inflammatory cytokines relevant for the development of atherosclerosis and diabetes. Pre-adipocytes were cultured and differentiated into mature adipocytes in vitro. Adipocytes and pre-adipocytes were incubated with infective and heat-inactivated Chlamydia pneumoniae, cytomegalovirus (CMV), adenovirus (Ad) subtypes 2 and 36, influenza A and respiratory syncitial virus (RSV). After 48 h, adiponectin, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) and plasminogen activator inhibitor-1 (PAI-1) were measured in supernatants. Infection of adipocytes with Ad-36, CMV and RSV resulted in increased IL-6 production from 192+/-22 pg ml(-1) (uninfected) to 1030+/-86 pg ml(-1), 838+/-59 pg ml(-1) and 1241+/-191 pg ml(-1), respectively (all P<0.01 vs control). In addition, Ad-36 infection slightly reduced PAI production in adipocytes (285+/-26.8 ng ml(-1) vs uninfected: 477+/-71.2 ng ml(-1); P=0.05) and pre-adipocytes (709+/-43.3 ng ml(-1) vs uninfected: 1071+/-71.8 ng ml(-1); P<0.01). In contrast, human Ad type 2 did not exert any effect on IL-6 or PAI production. None of the microorganisms induced significant changes in adiponectin and/or TNF-alpha production. Adipocytes can be infected with several microorganisms in vitro. Infection of adipocytes with Ad-36, but not Ad-2 leads to increased production of IL-6 which might contribute to chronic low-grade inflammation, a process known to be involved in the development of cardiovascular diseases and type 2 diabetes. Background: Abdominal obesity plays an important role in the development of insulin resistance, diabetes mellitus and atherosclerosis. The exact pathophysiological mechanisms are unclear but adipocyte dysfunction is thought to be crucial. Infections are associated with the development of atherosclerosis as well as diabetes. In this study we investigated whether adipocytes can be infected and whether this results in production of inflammatory cytokines relevant for the development of atherosclerosis and diabetes. Methods: Pre-adipocytes were cultured and differentiated into mature adipocytes in vitro . Adipocytes and pre-adipocytes were incubated with infective and heat-inactivated Chlamydia pneumoniae , cytomegalovirus (CMV), adenovirus (Ad) subtypes 2 and 36, influenza A and respiratory syncitial virus (RSV). After 48 h, adiponectin, interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and plasminogen activator inhibitor-1 (PAI-1) were measured in supernatants. Results: Infection of adipocytes with Ad-36, CMV and RSV resulted in increased IL-6 production from 192±22 pg ml −1 (uninfected) to 1030±86 pg ml −1 , 838±59 pg ml −1 and 1241±191 pg ml −1 , respectively (all P <0.01 vs control). In addition, Ad-36 infection slightly reduced PAI production in adipocytes (285±26.8 ng ml −1 vs uninfected: 477±71.2 ng ml −1 ; P =0.05) and pre-adipocytes (709±43.3 ng ml −1 vs uninfected: 1071±71.8 ng ml −1 ; P <0.01). In contrast, human Ad type 2 did not exert any effect on IL-6 or PAI production. None of the microorganisms induced significant changes in adiponectin and/or TNF-α production. Conclusions: Adipocytes can be infected with several microorganisms in vitro . Infection of adipocytes with Ad-36, but not Ad-2 leads to increased production of IL-6 which might contribute to chronic low-grade inflammation, a process known to be involved in the development of cardiovascular diseases and type 2 diabetes. |
| Audience | Academic |
| Author | Diepersloot, R.J.A Bouter, K.P Bouwman, J.J.M Visseren, F.L.J |
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| Copyright | Springer Nature Limited 2008 2008 INIST-CNRS COPYRIGHT 2008 Nature Publishing Group Copyright Nature Publishing Group Jun 2008 |
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| Issue | 6 |
| Keywords | infection TNF-α adipocytes IL-6 adenovirus Adipocyte Obesity Adenoviridae Nutrition Cytokine Nutrition disorder Metabolic diseases Inflammation In vitro Virus Infection Interleukin 6 Nutritional status Tumor necrosis factor α |
| Language | English |
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| PublicationTitle | International Journal of Obesity |
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| PublicationYear | 2008 |
| Publisher | Nature Publishing Group UK Nature Publishing Nature Publishing Group |
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start-page: 464 year: 1997 ident: BFijo200836_CR37 publication-title: Obes Res doi: 10.1002/j.1550-8528.1997.tb00672.x – volume: 63 start-page: 582 year: 2004 ident: BFijo200836_CR29 publication-title: Cardiovasc Res doi: 10.1016/j.cardiores.2004.05.001 – volume: 84 start-page: 319 year: 2000 ident: BFijo200836_CR13 publication-title: Thromb Haemost doi: 10.1055/s-0037-1614014 – volume: 131 start-page: 2794S year: 2001 ident: BFijo200836_CR18 publication-title: J Nutr doi: 10.1093/jn/131.10.2794S – volume: 25 start-page: 990 year: 2001 ident: BFijo200836_CR20 publication-title: Int J Obes Relat Metab Disord doi: 10.1038/sj.ijo.0801668 – volume: 31 start-page: 359 year: 1999 ident: BFijo200836_CR53 publication-title: Horm Metab Res doi: 10.1055/s-2007-978754 – volume: 34 start-page: 1738 year: 1999 ident: BFijo200836_CR14 publication-title: J Am Coll Cardiol doi: 10.1016/S0735-1097(99)00410-6 – volume: 280 start-page: E827 year: 2001 ident: BFijo200836_CR48 publication-title: Am J 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| SubjectTerms | Abdominal Fat - cytology Abdominal Fat - metabolism Adenoviridae Adenovirus Adenovirus Infections, Human - complications Adenovirus Infections, Human - metabolism adipocytes Adipocytes - metabolism Adipocytes - virology adiponectin Adiponectin - biosynthesis atherosclerosis Atherosclerosis - etiology Biological and medical sciences Cardiovascular diseases cell differentiation Cells, Cultured Chlamydophila Infections - complications Chlamydophila Infections - metabolism Chlamydophila pneumoniae Complications and side effects cultured cells cytokines Cytomegalovirus Cytomegalovirus Infections - complications Cytomegalovirus Infections - metabolism diabetes mellitus Diabetes Mellitus - etiology Diagnosis Epidemiology Fat cells Health aspects Health Promotion and Disease Prevention human cell lines Humans in vitro studies In Vitro Techniques Infection Inflammation Influenza A virus Influenza, Human - complications Influenza, Human - metabolism interleukin-6 Interleukin-6 - biosynthesis Internal Medicine Medical sciences Medicine Medicine & Public Health Metabolic Diseases Microorganisms Obesity original-article pathophysiology Plasminogen Activator Inhibitor 1 - biosynthesis plasminogen activator inhibitor-1 preadipocytes Public Health Respiratory syncitial virus Respiratory Syncytial Virus Infections - complications Respiratory Syncytial Virus Infections - metabolism Risk factors Sexually transmitted diseases STD tumor necrosis factor-alpha Tumor Necrosis Factor-alpha - biosynthesis vertebrate viruses |
| Title | Infection-induced inflammatory response of adipocytes in vitro |
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