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      Improved recovery from spinal cord injury in rats with chronic parvovirus serotype-1a infection

      1 , * , 1 , 1 , *
      Spinal Cord
      Nature Publishing Group

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          A vendor informed us that rats shipped to us and used by us in a spinal cord contusion injury experiment were infected by rat parvovirus type 1a (RPV-1a). Our aim was therefore to determine whether this infection may have altered locomotor recovery or tissue pathology.


          Stockholm, Sweden.


          We induced a moderate contusion injury of the spinal cord in rats received from an (unknown to us) RPV-1a-contaminated facility. We compared the hind limb locomotor function between RPV-1a-infected rats and non-infected controls with the same spinal cord lesions, obtained before (historical control), as well as after infection (future controls). Histologically, we assessed spinal tissue sparing, astrocyte reactivity and the amount of macrophages/activated microglia.


          RPV-1a-infected rats had significantly better hind limb locomotor recovery compared with both ‘historical' and ‘future' controls. We also observed significantly better tissue sparing and axonal sparing around the injury site, as well as significant reductions in macrophages/activated microglia and astrocyte reactivity in the spinal cords of RPV-1a-infected rats.


          The results stress the importance of knowing the health status of animals used to study central nervous system trauma and support the notion that acquired infections, even if asymptomatic, may alter response to injury in mammals. Furthermore, the results demonstrate that virus infections may have positive effects on functional recovery after spinal cord injury and indicate that RPV-1a infection may be neuroprotective by dampening secondary damage.

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          Most cited references12

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          Immune surveillance in the central nervous system

          Despite being protected by the blood-brain barrier, the CNS must constantly be monitored for insult or pathogen invasion. In this review, the authors illustrate the molecular and cellular players that preside over this surveillance of the brain and spinal cord.
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            The impact of parasite infections on the course of multiple sclerosis.

            Previously, we demonstrated that helminth-infected MS patients showed significantly lower number of relapses, reduced disability scores, and lower MRI activity compared to uninfected MS subjects. In the current study, 12 patients with diagnosis of relapsing remitting MS presenting parasite infections were prospectively followed during 90 months; due to exacerbation of helminth-infection symptoms after 63 months of follow-up, 4 patients received anti-parasite treatment. Helminth-infection control was associated with significant increase in clinical and radiological MS activities. Moreover, these patients showed significant increase in the number of IFN-γ and IL-12 producing cells, and a fall in the number of TGF-β and IL-10 secreting cells, as well as CD4+CD25+FoxP3+ Treg cells evident 3 months after anti-helminth treatment began. These new observations on parasite infections associated to MS indicate that parasite regulation of host immunity can alter the course of MS. Copyright © 2011 Elsevier B.V. All rights reserved.
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              Systemic infection and inflammation in acute CNS injury and chronic neurodegeneration: underlying mechanisms.

              We have all at some time experienced the non-specific symptoms that arise from being ill following a systemic infection. These symptoms, such as fever, malaise, lethargy and loss of appetite are often referred to as "sickness behavior" and are a consequence of systemically produced pro-inflammatory mediators. These inflammatory mediators signal to the brain, leading to activation of microglial cells, which in turn, signal to neurons to induce adaptive metabolic and behavioral changes. In normal healthy persons this response is a normal part of our defense, to protect us from infection, to maintain homeostasis and causes no damage to neurons. However, in animals and patients with chronic neurodegenerative disease, multiple sclerosis, stroke and even during normal aging, systemic inflammation leads to inflammatory responses in the brain, an exaggeration of clinical symptoms and increased neuronal death. These observations imply that, as the population ages and the number of individuals with CNS disorders increases, relatively common systemic infections and inflammation will become significant risk factors for disease onset or progression. In this review we discuss the underlying mechanisms responsible for sickness behavior induced by systemic inflammation in the healthy brain and how they might be different in individuals with CNS pathology.

                Author and article information

                Spinal Cord
                Spinal Cord
                Spinal Cord
                Nature Publishing Group
                July 2016
                22 December 2015
                : 54
                : 7
                : 517-520
                [1 ]Department of Neuroscience, Karolinska Institutet , Stockholm, Sweden
                Author notes
                [* ]Department of Neuroscience, Karolinska Institutet , Retzius väg 8, B2:4, Stockholm 171 77, Sweden. E-mail: Jacob.kjell@ 123456ki.se
                [* ]INCF, Karolinska Institutet , Nobels väg 15A, Stockholm 17177, Sweden. E-mail: Mathew@ 123456incf.org

                Current address: Department of Physiological Genomics, Ludwig-Maximilians-Universität München (LMU), 80336 Munich, Germany.


                Current address: INCF, Karolinska Institutet, Stockholm 171 77, Sweden.

                Copyright © 2016 International Spinal Cord Society

                This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/4.0/

                : 24 August 2015
                : 12 October 2015
                : 18 October 2015
                Original Article



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