Human Monocytes - CD14, CD16 - Ziegler-Heitbrock


Change in gut microbiota is correlated with alterations in the surface molecule expression of monocytes after Roux-en-Y gastric bypass surgery in obese type 2 diabetic patients.


Objectives: Persistent low-grade chronic inflammation is common in type 2 diabetes (T2D) and obesity. To date, the underlying molecular mechanism is not well understood. In this study, we aimed to investigate gut microbiota and the expression of monocyte surface molecules in obese T2D subjects who underwent Roux-en-Y gastric bypass (RYGB) surgery. Methods: Twenty-four T2D patients were enrolled. Gut microbiota was assessed by measuring bacterial DNA. The phenotypes and biological functions of monocytes, and the expression of monocyte surface molecules were examined by flow cytometry. Results: RYGB led to significant alterations in the phenotypes of monocytes. Moreover, the ability of monocyte migration was significantly decreased after RYGB (P<0.05), which was consistent with reduced Chemokine-receptors CCR2 expression of CD14+CD16+ monocytes (P<0.05) and CX3CR1 expression of the three monocytes subsets (P<0.05). RYGB also resulted in a shift of gut microbiota in the obese T2D patients. Spearmans rank correlation coefficient showed a link between gut microbiota and monocyte subsets where the increased Bacteroidetes was negatively correlated with the variation of CD14dimCD16+ monocyte percentage (r=-0.477, P<0.05). Furthermore, the decreased counts of Escherichia were positively correlated with the variation of TNF-α secretion (r=0.442, P<0.05) and TLR4 (r=0.425, P<0.05) expression onCD14+CD16+ monocytes. Conclusions: This study, for the first time, demonstrated a link between the changes in gut microbiota and alterations in both phenotypes and functions of monocytes after RYGB, which may contribute significantly to the low-grade chronic inflammation in obese T2D patients.

Authors: Chen H, Qian L, Lv Q, Yu J, Wu W, Qian H.
Journal: Am J Transl Res. 2017 Mar 15;9(3):1243-1254
Year: 2017
PubMed: Find in PubMed