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

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Research Article

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

Claus Vinter B Hviid1,2,3*, Are Hugo Pripp4, Ansgar O Aasen1,2 and Claus Danckert-Krohn1
1Institute for Surgical Research, Oslo University Hospital–HF, Rikshospitalet, 0027 Oslo, Norway
2Institute of Clinical Medicine, Faculty of Medicine, Oslo University, Blindern, 0318 Oslo, Norway
3Department of Anesthesia, Operation, and Intensive Care, Vestre Viken Hospital Trust, Drammen Sygehus, 3004 Drammen, Norway
4Department of Biostatistics, Epidemiology and Health Economics, Oslo University Hospital–HF, Ullevål, 0424 Oslo, Norway
Corresponding Author : Claus Vinter B Hviid
Institute for Surgical Research
Oslo University Hospital–HF, Rikshospitalet
P.O. Box 4950 Nydalen, 0424 Oslo, Norway
Tel: +47 41178329
E-mail: Claus.vinter@rr-research.no
Received August 30, 2014; Accepted October 28, 2014; Published October 31, 2014
Citation: Hviid CV, Pripp AH, Aasen AO, Danckert-Krohn C (2014) Postoperative Accumulation of Cyr61/CCN1 in Surgical Wound Fluid Precedes Cytokine Activation and is Disparate from Systemic Alterations. J Infect Dis Ther 2:181. doi:10.4172/2332-0877.1000181
 
Copyright: © 2014 Hviid CVB, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
 
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Abstract

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.

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