DIABETES-INDUCED IMPAIRMENT OF MACROPHAGE CYTOKINE RELEASE IN A RAT MODEL - POTENTIAL ROLE OF SERUM-LIPIDS

Diabetes (type I and type II) affects approximately 13 million people in the United States. Delayed and incomplete healing of wounds can be a major problem for diabetic patients. Macrophages are an important ce ll in the complex process of wound repair representing the major sourc e of cytokines throughout the wound healing process. Cytokines mediate many of the cellular responses critical to timely wound repair. It ha s been suggested that diabetes impairs wound healing through disruptio n of local cytokine production. We previously demonstrated that platel et-derived growth factor B chain (PDGF-B) levels are deficient at the wound site of diabetic rats. In the present study, we measured the lev els of several marker cytokines released from cultured peritoneal macr ophages of diabetic, nondiabetic hyperlipidemic, and normal rats. The diabetic condition was associated with a generalized reduction of macr ophage cytokine release. Nondiabetic hyperlipidemic animals demonstrat ed similar cytokine reduction supporting the hypothesis that elevated serum lipids are the primary determinants of diabetes-induced reductio ns in macrophage cytokine release. Thus, manipulation of serum lipids may be a therapeutically useful modality for controlling macrophage cy tokine release in the inflammatory and/or wound environment.