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

Maqsood M Elahi1, Bashir M Matata

  • 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.

ISRN Inflammation
|September 20, 2013
PubMed

Insights

Diabetes increases pro-inflammatory cytokine release from granulocytes (PMN), which is reduced by nitric oxide (NO). Mononuclear cells (PBMCs) show enhanced activity in diabetes, unaffected by NO.

Area of Science:

  • Immunology
  • Endocrinology
  • Molecular Biology

Background:

  • The role of blood granulocytes in releasing proinflammatory cytokines during diabetes is not fully understood.
  • Diabetes mellitus may alter cytokine production by immune cells, potentially influenced by nitric oxide (NO).

Purpose of the Study:

  • To investigate the effect of type-II diabetes on cytokine production by polymorphonuclear cells (PMN) and peripheral blood mononuclear cells (PBMCs).
  • To determine if nitric oxide (NO) modulates diabetes-induced cytokine production in these cells.

Main Methods:

  • Isolated PMN and PBMCs from diabetic and non-diabetic individuals were incubated with varying concentrations of S-nitroso-N-acetylpenicillamine (SNAP) and lipopolysaccharides (LPS).
  • Cytokine levels (TNF-α and IL-8) in supernatants were quantified using sandwich ELISA.

Main Results:

  • PMN from diabetic subjects showed significantly increased TNF-α and IL-8 production, which was concentration-dependently inhibited by exogenous NO.
  • PBMC activity, when stimulated with LPS, was enhanced in diabetic individuals but not affected by NO.

Conclusions:

  • Granulocyte activation and their contribution to diabetes complications are modulated by NO bioavailability.
  • Diabetes mellitus impacts cytokine production differently in PMN and PBMCs, with NO playing a regulatory role primarily in PMN.

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