INTRODUCTION: Cardiovascular complications are the leading cause of mortality in type 2 diabetes (T2DM), in which onset and progression of atherosclerosis is linked to chronic inflammation. Activation status of innate immune cells (granulocytes [Gc], monocytes [Mc]), as reflected by increased CD11b, CD66b, and other surface markers, increases their endothelial and cytokines/chemokines release. Whereas this inflammatory activation seems inversely related to poor glycemic control, the effect of acute spontaneous hyperglycemia on innate immune cell activation remains unclear. METHODS: Expression of key markers (CD11b, CD14, CD16, CD62L, and CD66b) was therefore determined by flow cytometry on whole blood of healthy subjects and patients with T2DM with spontaneous fasting euglycemia or hyperglycemia both at baseline and after 30, 90, and 240 minutes of incubation at room temperature. RESULTS: Hyperglycemic patients with T2DM had significantly higher Gc and Mc CD11b and Gc CD66b surface mean fluorescence intensity compared with the euglycemic patients with T2DM whose values were similar to those of the healthy controls. CD16 expression in CD14+CD16+ Mc was elevated in all patients with T2DM, regardless of glycemic levels. CONCLUSION: Our data suggest that whereas the presence of diabetes per se may have a proinflammatory effect, hyperglycemia seems to further acutely exacerbate innate cell inflammatory status and their consequent endothelial adhesion and vascular damage potential.
INTRODUCTION:Cardiovascular complications are the leading cause of mortality in type 2 diabetes (T2DM), in which onset and progression of atherosclerosis is linked to chronic inflammation. Activation status of innate immune cells (granulocytes [Gc], monocytes [Mc]), as reflected by increased CD11b, CD66b, and other surface markers, increases their endothelial and cytokines/chemokines release. Whereas this inflammatory activation seems inversely related to poor glycemic control, the effect of acute spontaneous hyperglycemia on innate immune cell activation remains unclear. METHODS: Expression of key markers (CD11b, CD14, CD16, CD62L, and CD66b) was therefore determined by flow cytometry on whole blood of healthy subjects and patients with T2DM with spontaneous fasting euglycemia or hyperglycemia both at baseline and after 30, 90, and 240 minutes of incubation at room temperature. RESULTS:Hyperglycemicpatients with T2DM had significantly higher Gc and McCD11b and Gc CD66b surface mean fluorescence intensity compared with the euglycemic patients with T2DM whose values were similar to those of the healthy controls. CD16 expression in CD14+CD16+ Mc was elevated in all patients with T2DM, regardless of glycemic levels. CONCLUSION: Our data suggest that whereas the presence of diabetes per se may have a proinflammatory effect, hyperglycemia seems to further acutely exacerbate innate cell inflammatory status and their consequent endothelial adhesion and vascular damage potential.
Authors: Jaime S Rosa; Rebecca L Flores; Stacy R Oliver; Andria M Pontello; Frank P Zaldivar; Pietro R Galassetti Journal: J Appl Physiol (1985) Date: 2009-12-10
Authors: Kyrill S Rogacev; Christof Ulrich; Lutz Blömer; Florian Hornof; Katrin Oster; Maren Ziegelin; Bodo Cremers; Yvonne Grenner; Jürgen Geisel; Axel Schlitt; Hans Köhler; Danilo Fliser; Matthias Girndt; Gunnar H Heine Journal: Eur Heart J Date: 2009-08-17 Impact factor: 29.983
Authors: P R Galassetti; K Iwanaga; A M Pontello; F P Zaldivar; R L Flores; J K Larson Journal: Am J Physiol Endocrinol Metab Date: 2005-12-06 Impact factor: 4.310
Authors: Kyrill S Rogacev; Sarah Seiler; Adam M Zawada; Birgit Reichart; Esther Herath; Daniel Roth; Christof Ulrich; Danilo Fliser; Gunnar H Heine Journal: Eur Heart J Date: 2010-10-12 Impact factor: 29.983
Authors: Estella A Newcombe; Judith Camats-Perna; Mallone L Silva; Nicholas Valmas; Tee Jong Huat; Rodrigo Medeiros Journal: J Neuroinflammation Date: 2018-09-24 Impact factor: 8.322
Authors: Michaela Šiklová; Eva Krauzová; Barbora Svobodová; Jana Kračmerová; Marek Štěpán; Michal Koc; Vladimír Štich; Lenka Rossmeislová Journal: Mediators Inflamm Date: 2019-03-11 Impact factor: 4.711