The effect of hyperglycaemia on the macrophages in the cell culture

Abstract

Background: The availability of glucose in tissue has a role in macrophages polarization into an inflammatory phenotype. The over nutrition condition such as hyperglycemia induces macrophage infiltration especially the inflammatory macrophages. The aim of this study is to analyse the effect of hyperglycemia condition on cytokines production by human monocytes-derived macrophages. Materials and methods: Monocyte cells that obtained from peripheral blood mononuclear cells isolation from donors were incubated for 6 days in 37°C, 5% CO2. On day 4, the stimulating factors such as lipopolysaccharide (LPS) and interferon (INF)-ɤ were added to activate monocytes into macrophages. Then on day 6, two doses of glucose; either normal or high doses along with low or high dose of LPS were given for 24 hours, followed by collecting the culture media and cells then stored at −80°C until assayed. Results: There was significantly different of TNF-α level among groups, with highest level found in group with high dose glucose plus high dose LPS. However, the concentration of IL-6 among groups was not significantly different. Conclusions: Macrophages treated with high dose glucose plus high dose LPS significantly increased TNF-α production, but not for IL-6.

A2BAR Antagonism Decreases the Glomerular Expression and Secretion of Chemoattractants for Monocytes and the Pro-Fibrotic M2 Macrophages Polarization during Diabetic Nephropathy

“…A growing and important number of investigations have shown that the function of the immune system is altered in DM, with hyperglycemia being one of the factors responsible for this dysfunction [ 79 , 80 , 81 , 82 , 83 , 84 ]. Hyperglycemia can modify the activity of various leukocytes, including monocytes/MΦs [ 85 , 86 ]. Both in vitro and in vivo studies indicate that chronic hyperglycemia increased polarization of M2 MΦs in diabetic mice and in bone marrow-derived MΦs exposed to high glucose concentrations [ 79 , 87 , 88 ], which would contribute to the progression of tissue fibrosis in DM.…”

Hyperglycemia Aggravates Blood–Brain Barrier Disruption Following Diffuse Axonal Injury by Increasing the Levels of Inflammatory Mediators through the PPARγ/Caveolin-1/TLR4 Pathway

“…Experimental studies have shown that a hyperglycemic condition activates the production of IL-1, IL-6, and TNF-𝛼 [39][40][41] . All these in ammatory factors have been reported to be related to secondary axonal injury.…”