Gene Expression Profile of Innate Immune Cells in Type-2 Diabetes

Objectives: Type 2 Diabetes Mellitus (T2D) is a health problem of increasing concern that affects people worldwide. There is evidence that individuals with uncontrolled T2D have an unbalanced ratio of inflammatory and pro-resolution molecules and receptors. The goal of this study was to further the understanding of the inflammatory and pro-resolution gene expression profile of T2D from isolated human innate immune cells (monocytes and neutrophils).
Methods: Peripheral blood was collected from healthy and type 2 diabetic individuals. Monocytes and neutrophils were isolated using histopaque method. Total RNA was extracted from the cells and was transcribed to cDNA using a PCR. Gene expression of 15 inflammatory and 11 pro-resolution genes was evaluated and expressed by fold change method (2^-∆∆CT) of quantitative PCR.
Results: For anti-inflammatory and pro-resolution genes, ChemR23 and ARG1 gene expression was elevated in monocytes from T2D subjects as compared to healthy controls (3.12±0.51, 4.44±1.22 fold respectively [p<0.05]). GPR32, MHC-II, IL-10, and TIMD4 gene expression was reduced in T2D monocytes (0.21±0.07, 0.59±0.20, 0.28±0.07, 0.25±0.08 fold respectively [p<0.05]). In T2D neutrophils, anti-inflammatory and pro-resolution genes ALX and c-Jun gene expression was elevated as compared to healthy controls (1.45±0.37, 1.61±0.48 fold respectively [p<0.05]). The majority of the expressions of the resolution and anti-inflammatory genes were down-regulated.
Conclusions: In both monocytes and neutrophils, there is a clear differential expression of pro-resolution and inflammation genes. These findings show that there is an unbalance in the expression of resolution and anti-inflammatory genes in T2D affected innate immune cells. These demonstrate that innate immune cells are influenced by the T2D hyper-inflammatory environment.