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Postoperative Accumulation of Cyr61/CCN1 in Surgical Wound Fluid Precedes Cytokine Activation and is Disparate from Systemic Alterations

Claus Vinter B Hviid, Are Hugo Pripp, Ansgar O Aasen and Claus Danckert-Krohn

Background: Cysteine-rich protein 61 (Cyr61/CCN1) is a multifunctional matricellular protein that has recently emerged as a potential player in injury-repair mechanisms involving the regulation of inflammatory responses. Experimental research has revealed the pro-inflammatory effects and chemotactic capacities of this protein, and clinical investigations have found it to be elevated in patients with chronic inflammatory conditions. However, its regulation at sites of acute tissue injury and inflammation in humans has not been investigated.
Methods: Ten otherwise healthy patients undergoing major orthopedic surgery for idiopathic thoracic scoliosis were recruited to the study. Fluid from the surgical drain and systemic blood was collected at 0, 1, 2, 4, and 6 hours following wound closure and analyzed for CCN1 levels, neutrophil counts, selected cytokines, and markers of primary hemostasis activation.
Results and Conclusions: In the drained fluid, CCN1 levels increased from 1 hour after wound closure, whereas its levels remained unaltered in systemic circulation. The platelet activation marker soluble P-selectin increased in the drained fluid but not in the systemic blood, resulting in a strong correlation between CCN1 and soluble P-selectin in the drained fluid (r=0.649, p=0.042). Levels of interleukin-6 and granulocyte-colony stimulating factor were elevated in the drained fluid only from two hours after wound closure, and neutrophil counts, tumor necrosis factor– alpha, interleukin-8 and interleukin-10 were elevated from 4 hours after wound closure. The present study demonstrated that CCN1 accumulates in fluid drained from surgical wounds following major surgery. It revealed that CCN1 levels increased simultaneously with soluble P-selectin, and prior to those of classical cytokine mediators, which suggests a connection between platelet activation and CCN1 accumulation. Collectively, these data suggest that CCN1 may play a role in the acute phases of human tissue injury and support its role as an early participant in acute inflammation in humans.