The in vitro Effects of Different Concentrations of Glucose on Innate Immune Cell Activation

In diabetes the duration, frequency and magnitude of repeated hyperglycemia is proportional to the incidence/severity of cardiovascular complications. While a chronic subclinical inflammatory state is the proposed underlying pathogenetic mechanisms, the biochemical details of the interactions between hyperglycemia and inflammation remain unclear. There are known alterations in the immune system of people living with diabetes including the elevated levels of inflammatory markers. We hypothesize that there would be an effect of different concentrations of glucose on innate immune cell (granulocyte, Gc, and monocyte, Mc) activation. Whole blood from eight young, healthy males were incubated with 0 or 22mM glucose for 0, 30, 60, 90, and 240 min. The 22mM concentration is a very high hyperglycemic level periodically experienced by very poorly controlled diabetic patients. Flow cytometry was used to determine Gc and Mc activation (CD11, CD14, CD16, CD62L, CD66b). We observed that under hyperglycemic conditions, expression of most measured markers was quantitatively higher in cells exposed to hyperglycemia. This difference was statistically significant for CD11b at 90 min in both Gc and Mc, and for CD66b in Gc. Our data suggest a direct pro‐inflammatory effect of excess glucose on cells of the innate immune system, potentially contributing to the increase of systemic inflammation reported in diabetes.