Neuroprotective Effects of Interleukin-10 Following Excitotoxic Spinal Cord Injury

Brewer, Kori L.; Bethea, John R.; Yezierski, Robert P.

doi:10.1006/exnr.1999.7173

Cited by 139 publications

(102 citation statements)

References 35 publications

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“…Moreover, this model of injury results in behavioral sequelae that include allodynia, hyperalgesia, and spontaneous pain behaviors. Using the excitotoxic SCI model, studies have examined modalities that may limit secondary damage and provide antinociception for chronic pain (31,32,51,52). However, there have been no studies showing alleviation of chronic pain following ES cell transplant.…”

Section: Discussionmentioning

confidence: 99%

“…Each animal received 0.6 µL of 125 mM QUIS (Sigma) in PBS injected over 3 min (three tracks of 0.2 µL separated by 0.3 mm, parallel to the long axis of the cord). This amount of QUIS produces overgrooming behavior in ~60% of animals according to previous studies (31,32). After microinjections, muscles were sutured in layers and the overlying skin was closed with staples.…”

Section: Animal Surgerymentioning

confidence: 91%

“…Serial reconstruction of the lesion was done as described previously (32). For lesion analysis, serial cross-sections of 50 µm were collected in 0.1 M PBS and mounted on superfrost microscope slides (Fisher Scientific, Pittsburgh, PA, USA).…”

Section: Lesion Analysismentioning

confidence: 99%

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Predifferentiated Embryonic Stem Cells Prevent Chronic Pain Behaviors and Restore Sensory Function Following Spinal Cord Injury in Mice

Hendricks

Pak

Owensby

et al. 2006

Mol Med

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Embryonic stem (ES) cells have been investigated in repair of the CNS following neuronal injury and disease; however, the efficacy of these cells in treatment of postinjury pain is far from clear. In this study, we evaluated the therapeutic potential of predifferentiated mouse ES cells to restore sensory deficits following spinal cord injury (SCI) in mice. The pain model used unilateral intraspinal injection of quisqualic acid (QUIS) into the dorsal horn between vertebral levels T13 and L1. Seven days later, 60,000 predifferentiated ES cells or media were transplanted into the site of the lesion. Histological analysis at 7, 14, and 60 days posttransplantation revealed that animals receiving ES cell transplants suffered significantly less tissue damage than animals receiving media alone. Transplanted cells provided immediate effects on both spontaneous and evoked pain behaviors. Treatment with ES cells resulted in 0% (n = 28) excessive grooming behavior versus 60% (18 of 30) in media-treated animals. In the acetone test (to assess thermal allodynia), mice recovered to preinjury levels by 12 days after ES cell transplant, whereas control animals injected with media after SCI did not show any improvement up to 60 days. Similarly, the von Frey test (to assess mechanical allodynia) and the formalin test (to assess nociceptive hyperalgesia) showed that transplantation of predifferentiated ES cells significantly reduced these pain behaviors following injury. Here we show that predifferentiated ES cells act in a neuroprotective manner and provide antinociceptive and therapeutic effects following excitotoxic SCI.

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Section: Discussionmentioning

confidence: 99%

Section: Animal Surgerymentioning

confidence: 91%

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Predifferentiated Embryonic Stem Cells Prevent Chronic Pain Behaviors and Restore Sensory Function Following Spinal Cord Injury in Mice

Hendricks

Pak

Owensby

et al. 2006

Mol Med

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“…Neutralization of IFN-␥ activity restored IL-10 expression by human herpes virus type 6-infected cells (36). Therefore, the increased levels of IL-10 may further diminish an effective host response to MHV by contributing to the inhibition of CNS inflammation as well as inhibiting cellular function as has been suggested to occur in experimental autoimmune encephalomyelitis and other models of CNS inflammation (37)(38)(39)(40)(41).…”

Section: Discussionmentioning

confidence: 99%

Expression of Mig (Monokine Induced by Interferon-γ) Is Important in T Lymphocyte Recruitment and Host Defense Following Viral Infection of the Central Nervous System

Liu

Armstrong²,

Hamilton³

et al. 2001

The Journal of Immunology

136

140

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Induction of a Th1 immune response against viral infection of the CNS is important in contributing to viral clearance. The present studies demonstrate a role for the T cell chemoattractant chemokine Mig (monokine induced by IFN-γ) in contributing to a Th1 response against mouse hepatitis virus infection of the CNS. Analysis of the kinetics of Mig expression revealed mRNA transcripts present at days 7 and 12 postinfection (p.i.) but not early (day 2) or late (day 35) in the infection. To determine functional significance, mouse hepatitis virus-infected mice were treated with anti-Mig antisera, and the severity of disease was evaluated. Such treatment resulted in a marked increase in mortality that correlated with a >3 log increase in viral burden within the brains as compared with control mice treated with normal rabbit serum. Anti-Mig-treated mice displayed a significant decrease (p < 0.005) in CD4+ and CD8+ T cell recruitment into the CNS as compared with normal rabbit serum-treated mice. In addition, anti-Mig treatment resulted in a significant decrease (p < 0.05) in levels of IFN-γ and IFN-β that coincided with increased (p < 0.02) expression of the anti-inflammatory Th2 cytokine IL-10 within the CNS. Collectively, these data indicate that Mig is important in contributing to host defense by promoting a protective Th1 response against viral infection of the CNS.

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“…IL‐10 has been demonstrated to promote functional recovery in SCI models in rats66, 67, 68, 69, 72, 73, 74 and mice 58, 64, 65, 70, 71. IL‐10 affects inflammation through regulation of activation of microglia/macrophages70, 71 and astrocytes,72 as well as reducing the production of TNF‐α,72, 73 IL‐1β, S100β, and inducible nitric oxide synthase (iNOS) 65.…”

Section: Roles Of Inflammatory Cytokines In Sci Repairmentioning

confidence: 99%

Regulation of Inflammatory Cytokines for Spinal Cord Injury Repair Through Local Delivery of Therapeutic Agents

et al. 2018

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The balance of inflammation is critical to the repair of spinal cord injury (SCI), which is one of the most devastating traumas in human beings. Inflammatory cytokines, the direct mediators of local inflammation, have differential influences on the repair of the injured spinal cord. Some inflammatory cytokines are demonstrated beneficial to spinal cord repair in SCI models, while some detrimental. Various animal researches have revealed that local delivery of therapeutic agents efficiently regulates inflammatory cytokines and promotes repair from SCI. Quite a few clinical studies have also shown the promotion of repair from SCI through regulation of inflammatory cytokines. However, local delivery of a single agent affects only a part of the inflammatory cytokines that need to be regulated. Meanwhile, different individuals have differential profiles of inflammatory cytokines. Therefore, future studies may aim to develop personalized strategies of locally delivered therapeutic agent cocktails for effective and precise regulation of inflammation, and substantial functional recovery from SCI.

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Neuroprotective Effects of Interleukin-10 Following Excitotoxic Spinal Cord Injury

Cited by 139 publications

References 35 publications

Predifferentiated Embryonic Stem Cells Prevent Chronic Pain Behaviors and Restore Sensory Function Following Spinal Cord Injury in Mice

Predifferentiated Embryonic Stem Cells Prevent Chronic Pain Behaviors and Restore Sensory Function Following Spinal Cord Injury in Mice

Expression of Mig (Monokine Induced by Interferon-γ) Is Important in T Lymphocyte Recruitment and Host Defense Following Viral Infection of the Central Nervous System

Regulation of Inflammatory Cytokines for Spinal Cord Injury Repair Through Local Delivery of Therapeutic Agents

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