Table of Contents
ISRN Inflammation
Volume 2013, Article ID 531026, 3 pages
Research Article

Nitric Oxide-Dependent Regulation of Cytokines Release in Type-II Diabetes Mellitus

1Division of Cardiothoracic Surgery, Department of Surgery, Scott & White Memorial Hospital, Texas A&M Health Science Centre, 2401 S. 31st Street, Temple, TX 76508, USA
2Department of Clinical Research, The Liverpool Heart and Chest Hospital NHS Foundation Trust, Thomas Drive, Liverpool L14 3PE, UK

Received 5 December 2012; Accepted 17 January 2013

Academic Editors: J. M. Antony, A. M. Smith, and J. Voswinkel

Copyright © 2013 Maqsood M. Elahi and Bashir M. Matata. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The mechanism of release of proinflammatory cytokines by blood granulocytes in diabetes is unknown. We investigated whether diabetes mellitus affects the production of cytokines by granulocytes (PMN) and mononuclear cells (PBMCs) and whether this is modulated by NO. Isolated PMN and PBMC from with or without type-II diabetes mellitus were incubated at 37°C for 6 h with S-nitroso-N-acetylpenicillamine (SNAP) at 0, 1, and 100 μM with or without lipopolysaccharides (LPS) stimulation (1 μg/mL). Supernatants were assayed for tumor necrosis factor-α (TNF-α) and interleukin-8 (IL-8) by sandwich ELISA. Significant increases in TNF-α and IL-8 were observed only in PMN from diabetic subjects with or without LPS stimulation and that exogenous NO inhibited further production of cytokines in a concentration-dependent manner. However, activity of PBMC when stimulated with LPS was greatly enhanced by diabetes, but not affected by NO production. Hence, suggesting that granulocytes activation and participation in diabetes related complications is modulated by NO bioavailability.