Low Glucose Concentrations Induce a Similar Inflammatory Response in Monocytes from Type 2 Diabetic Patients and Healthy Subjects.
Francesco PiarulliGiovanni SartoreAnnalisa SechiDaniela BassoPaola FogarEliana GrecoEugenio RagazziAnnunziata LapollaPublished in: Oxidative medicine and cellular longevity (2017)
This study aims to assess the proinflammatory interleukin 1β (IL-1β) and anti-inflammatory IL-10 production by monocytes from 38 patients with type 2 diabetes and 31 controls in different glucose concentrations. Monocytes were incubated in low (2.5 mmol/L)-, normal (5.0 mmol/L)-, and high (20 mmol/L)-glucose conditions in the presence and absence of lipopolysaccharide (LPS). Monocytes from both patients and controls only produced a significant increase in IL-1β in low-glucose conditions (p < 0.01), and this phenomenon was amplified in the presence of LPS, while it was not seen in normal- or high-glucose conditions, not even in the presence of LPS stimulation. There was no increase in IL-10 production by monocytes from either diabetic patients or controls using whatever glucose concentrations, except when treated with LPS in normal-glucose conditions. These findings seem to suggest that low-glucose conditions induce an inflammatory response in monocytes in all individuals, as an intrinsic capacity of this cell line. On the other hand, monocytes only retain their anti-inflammatory ability in response to known inflammatory stimuli such as LPS, under normal-glucose concentrations. In conclusion, human monocytes express an inflammatory pattern in low-glucose conditions in vitro. This response could contribute to explaining the higher cardiovascular risk induced by hypoglycemia in diabetic patients.
Keyphrases
- inflammatory response
- anti inflammatory
- blood glucose
- dendritic cells
- peripheral blood
- lipopolysaccharide induced
- endothelial cells
- toll like receptor
- lps induced
- chronic kidney disease
- oxidative stress
- end stage renal disease
- high glucose
- blood pressure
- immune response
- skeletal muscle
- insulin resistance
- patient reported
- pluripotent stem cells