Anterior chamber associated immune deviation used as a neuroprotective strategy in rats with spinal cord injury
- Beatriz Pineda-Rodriguez,
- Diana Toscano-Tejeida,
- Elisa García–Vences,
- Roxana Rodriguez-Barrera,
- Adrian Flores-Romero,
- Daniela Castellanos-Canales
- Universidad Anáhuac,
- Facultad de Ciencias de la Salud,
- Universidad Nacional Autónoma de México,
- Departamento de Biología Celular y Fisiología,
- Universidad Michoacana de San Nicolas de Hidalgo,
- Laboratorio de Ecofisiología Animal
Open access
Publication Information
Output type
Original language
EnglishArticle number
e0188506Journal (Volume, Issue Number)
PLoS ONE (Volume 12, Issue 11)Publication milestones
- Published - 01/11/2017
Publication status
Publication IDs
- Scopus: 85036581354
- PubMed: 29190648
Abstract
The inflammatory response is probably one of the main destructive events occurring after spinal cord injury (SCI). Its progression depends mostly on the autoimmune response developed against neural constituents. Therefore, modulation or inhibition of this self-reactive reaction could help to reduce tissue destruction. Anterior chamber associated immune deviation (ACAID) is a phenomenon that induces immune-tolerance to antigens injected into the eye´s anterior chamber, provoking the reduction of such immune response. In the light of this notion, induction of ACAID to neural constituents could be used as a potential prophylactic therapy to promote neuroprotection. In order to evaluate this approach, three experiments were performed. In the first one, the capability to induce ACAID of the spinal cord extract (SCE) and the myelin basic protein (MBP) was evaluated. Using the delayed type hypersensibility assay (DTH) we demonstrated that both, SCE and MBP were capable of inducing ACAID. In the second experiment we evaluated the effect of SCE-induced ACAID on neurological and morphological recovery after SCI. In the results, there was a significant improvement of motor recovery, nociceptive hypersensitivity and motoneuron survival in rats with SCE-induced ACAID. Moreover, ACAID also up-regulated the expression of genes encoding for anti-inflammatory cytokines and FoxP3 but down-regulated those for pro-infla-matory cytokines. Finally, in the third experiment, the effect of a more simple and practical strategy was evaluated: MBP-induced ACAID, we also found significant neurological and morphological outcomes. In the present study we demonstrate that the induction of ACAID against neural antigens in rats, promotes neuroprotection after SCI.
