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Mediators of Inflammation
Volume 2016 (2016), Article ID 2684098, 15 pages
Research Article

Genetic Ablation of Soluble TNF Does Not Affect Lesion Size and Functional Recovery after Moderate Spinal Cord Injury in Mice

1Neurobiology Research, Institute of Molecular Medicine, J.B. Winsloewsvej 21, st, 5000 Odense C, Denmark
2Department of Diagnostics, Molecular Sleep Lab, Rigshospitalet, Nordre Ringvej 69, 2600 Glostrup, Denmark
3Department of Pathology, Department of Clinical Research, SDU Muscle Research Cluster, University of Southern Denmark, J.B. Winsloewsvej 15, 5000 Odense C, Denmark
4The Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, 1095 NW 14th Terrace, Miami, FL 33136, USA
5Department of Neurology, Odense University Hospital, J.B. Winsloewsvej 4, 5000 Odense C, Denmark
6Brain Research-Inter-Disciplinary Guided Excellence (BRIDGE), Department of Clinical Research, 5000 Odense C, Denmark

Received 8 August 2016; Revised 24 October 2016; Accepted 3 November 2016

Academic Editor: Ana Raquel Santiago

Copyright © 2016 Ditte Gry Ellman et al. 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.


Traumatic spinal cord injury (SCI) is followed by an instant increase in expression of the microglial-derived proinflammatory cytokine tumor necrosis factor (TNF) within the lesioned cord. TNF exists both as membrane-anchored TNF (mTNF) and as cleaved soluble TNF (solTNF). We previously demonstrated that epidural administration of a dominant-negative inhibitor of solTNF, XPro1595, to the contused spinal cord resulted in changes in Iba1 protein expression in microglia/macrophages, decreased lesion volume, and improved locomotor function. Here, we extend our studies using mice expressing mTNF, but no solTNF (), to study the effect of genetic ablation of solTNF on SCI. We demonstrate that TNF levels were significantly decreased within the lesioned spinal cord 3 days after SCI in mice compared to littermates. This decrease did, however, not translate into significant changes in other pro- and anti-inflammatory cytokines (IL-10, IL-1β, IL-6, IL-5, IL-2, CXCL1, CCL2, or CCL5), despite a tendency towards increased IL-10 and decreased IL-1β, TNFR1, and TNFR2 levels in mice. In addition, microglial and leukocyte infiltration, activation state (Iba1, CD11b, CD11c, CD45, and MHCII), lesion size, and functional outcome after moderate SCI were comparable between genotypes. Collectively, our data demonstrate that genetic ablation of solTNF does not significantly modulate postlesion outcome after SCI.