Fasting Glucose Level Modulates Cell Surface Expression of CD11b and CD66b in Granulocytes and Monocytes of Patients with Type II Diabetes

Horvath, Peter; Oliver, Stacy R.; Ganesan, Goutham; Zaldivar, Frank P.; Radom-Aizik, Shlomit; Galassetti, Pietro R.

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Fasting Glucose Level Modulates Cell Surface Expression of CD11b and CD66b in Granulocytes and Monocytes of Patients with Type II Diabetes

Published Date:

Aug 2013

Source:

J Investig Med. 61(6):972-977.

[PDF - 275.43 KB]

Details:

Personal Authors:

Horvath, Peter ; Oliver, Stacy R. ; Ganesan, Goutham ; Zaldivar, Frank P. ; Radom-Aizik, Shlomit ; ... More ▼

Keywords:

[+]

Pubmed ID:

23686079

Pubmed Central ID:

PMC3738167

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.

Document Type:

Journal Article

Collection(s):

CDC Public Access

Funding:

1UL1TS000153/TS/ATSDR CDC HHS/United States
K24 DK085223/DK/NIDDK NIH HHS/United States
K24 DK085223/DK/NIDDK NIH HHS/United States
M01 RR000827/RR/NCRR NIH HHS/United States
P01 HD048721/HD/NICHD NIH HHS/United States
P01HD048721/HD/NICHD NIH HHS/United States
T32 GM008620/GM/NIGMS NIH HHS/United States
UL1 RR031985/RR/NCRR NIH HHS/United States
UL1 TR000153/TR/NCATS NIH HHS/United States

Supporting Files:

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