Abstract

Monocytes express many cell surface markers indicative of their inflammatory and activation status. Whether these markers are affected by diabetes and its complications is not known and was investigated in this study. Blood was obtained from 22 nondiabetic and 43 diabetic subjects with a duration of diabetes >10 years, including 25 without and 18 with clinically significant complications. The number of CD45+CD14+ monocytes and the percentage expressing the proinflammatory marker CD16 were determined by flow cytometry. Other markers of monocyte activation and expression of chemokine receptors were also examined. The relationship between monocyte CD16 and clinical data, selected cytokines, and chemokines was also investigated. Diabetes had no effect on total white cell number but increased monocyte number. Diabetes also significantly decreased the number of CD16+ monocytes but only in those with diabetic complications. Other markers of monocyte activation status and chemokine receptors were not affected by diabetes or complications status. Diabetes induced plasma proinflammatory cytokines and they were lower in diabetic subjects with complications compared to those without complications. These results suggest that the circulating monocyte phenotype is altered by diabetic complications status. These changes may be causally related to and could potentially be used to predict susceptibility to diabetic complications.

Highlights

  • The complications of diabetes are responsible for much of its associated morbidity and mortality

  • The levels of circulating proinflammatory cytokines and chemokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL1β), and monocyte chemoattractant protein-1 (MCP-1) are commonly used as markers of inflammation, and they have been shown to be increased in diabetes [8,9,10]

  • CD68 is a marker for tissue macrophages, and CD11b is expressed by activated monocytes [6, 22, 23]

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Summary

Introduction

The complications of diabetes are responsible for much of its associated morbidity and mortality. The CD16− monocytes constitute a “classically activated” subset of monocytes which account for 80–90% of circulating monocytes in normal healthy individuals This population is increased in acute inflammation and is rapidly recruited to sites of infection [11,12,13]. The CD16+ monocytes constitute the “nonclassically activated” subset which makes up the remainder of the monocyte population This CD16+ population has a patrolling function to sense tissue injury, and Mediators of Inflammation is increased in ageing and chronic inflammatory disorders [11,12,13,14,15,16]. CD68 is a marker for tissue macrophages, and CD11b is expressed by activated monocytes [6, 22, 23]

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