ArticleJournal of investigative medicine : the official publication of the American Federation for Clinical Research2013
Fasting glucose level modulates cell surface expression of CD11b and CD66b in granulocytes and monocytes of patients with type 2 diabetes.
Article in Journal of investigative medicine : the official publication of the American Federation for Clinical Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Reliable discrimination of type 1 and type 2 diabetes by flow-through leukocyte-endothelium interactions exploiting advanced hydrodynamic detection parameters.Analytical and bioanalytical chemistry · 2026Article
- Metabolic features of neutrophilic differentiation of HL-60 cells in hyperglycemic environments.BMJ open diabetes research & care · 2024Article
- Does Genetic Predisposition Contribute to the Exacerbation of COVID-19 Symptoms in Individuals with Comorbidities and Explain the Huge Mortality Disparity between the East and the West?International journal of molecular sciences · 2021Review
- Circulating Monocyte and Lymphocyte Populations in Healthy First-Degree Relatives of Type 2 Diabetic Patients at Fasting and during Short-Term Hyperinsulinemia.Mediators of inflammation · 2019Article
- Inflammation: the link between comorbidities, genetics, and Alzheimer's disease.Journal of neuroinflammation · 2018Review
- Bioenergetic state regulates innate inflammatory responses through the transcriptional co-repressor CtBP.Nature communications · 2017Article
- Analysis of inflammatory cytokine and TLR expression levels in Type 2 Diabetes with complications.Scientific reports · 2017Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
introductionCardiovascular 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.
methodsExpression 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.
resultsHyperglycemic 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.
conclusionOur 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.
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