Details:

Alternative Title:
J Investig Med
Personal Author:
Horvath, Peter ; Oliver, Stacy R. ; Ganesan, Goutham ; Zaldivar, Frank P. ; Radom-Aizik, Shlomit ; ... More +
Horvath, Peter ; Oliver, Stacy R. ; Ganesan, Goutham ; Zaldivar, Frank P. ; Radom-Aizik, Shlomit ; Galassetti, Pietro R. ; Less -
Description:
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.|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.|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.|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.
Subject:
[+]
Adult
Antigens, CD
Article
Biomarkers
Blood Glucose
CD11b Antigen
Cell Adhesion Molecules
Diabetes Mellitus, Type 2
Fasting
Female
Gene Expression Regulation
Glucose
GPI-Linked Proteins
Granulocytes
Humans
Male
Membrane Proteins
Middle Aged
Monocytes
Surface Properties
Type II Diabetes

Source:
J Investig Med. 61(6):972-977
Pubmed ID:
23686079
Pubmed Central ID:
PMC3738167
Document Type:
Journal Article ;
Funding:
T32 GM008620/GM/NIGMS NIH HHS/United States ; K24 DK085223/DK/NIDDK NIH HHS/United States ; UL1 RR031985/RR/NCRR NIH HHS/United States ; U61 TS000153/TS/ATSDR CDC HHS/United States ; 1UL1TS000153/TS/ATSDR CDC HHS/United States ; ... More +
T32 GM008620/GM/NIGMS NIH HHS/United States ; K24 DK085223/DK/NIDDK NIH HHS/United States ; UL1 RR031985/RR/NCRR NIH HHS/United States ; U61 TS000153/TS/ATSDR CDC HHS/United States ; 1UL1TS000153/TS/ATSDR CDC HHS/United States ; P01HD048721/HD/NICHD NIH HHS/United States ; UL1 TR000153/TR/NCATS NIH HHS/United States ; M01 RR000827/RR/NCRR NIH HHS/United States ; P01 HD048721/HD/NICHD NIH HHS/United States ; Less -
Collection(s):
CDC Public Access
Main Document Checksum:
[+]
urn:sha256:5482b2cbea1dfb2e7bd221c160d8369be78f6c1d8a85cd716ddb4295c34dd80d
File Type:

Supporting Files

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