title: Absence of endogenous interleukin-10 enhances secondary inflammatory process after spinal cord compression injury in mice.
abstract: Interleukin-10 (IL-10) exerts a wide spectrum of regulatory activities in the immune and inflammatory response. The aim of this study was to investigate the role of endogenous IL-10 on the modulation of the secondary events in mice subjected to spinal cord injury induced by the application of vascular clips (force of 24 g) to the dura via a four-level T5-T8 laminectomy. IL-10 wild-type mice developed severe spinal cord damage characterized by oedema, tissue damage and apoptosis (measured by Annexin-V, terminal deoxynucleotidyltransferase-mediated UTP end labeling staining, Bax, Bcl-2, and Fas-L expression). Immunohistochemistry demonstrated a marked increase of localization of TNF-alpha, IL-1beta and S100beta, while western blot analysis shown an increased immunoreactivity of inducible nitric oxide synthase in the spinal cord tissues. The absence of IL-10 in IL-10 KO mice resulted in a significant augmentation of all the above described parameters. We have also demonstrated that the genetic absence of IL-10 worsened the recovery of limb function when compared with IL-10 wild-type mice group (evaluated by motor recovery score). Taken together, our results clearly demonstrate that the presence of IL-10 reduces the development of inflammation and tissue injury events associated with spinal cord trauma.
authors.affiliation: IRCCS Centro Neurolesi 'Bonino-Pulejo', Messina, Italy.
authors.forename: Tiziana
authors.initials: T
authors.lastname: Genovese
authors.forename: Emanuela
authors.initials: E
authors.lastname: Esposito
authors.forename: Emanuela
authors.initials: E
authors.lastname: Mazzon
authors.forename: Rosanna
authors.initials: R
authors.lastname: Di Paola
authors.forename: Rocco
authors.initials: R
authors.lastname: Caminiti
authors.forename: Placido
authors.initials: P
authors.lastname: Bramanti
authors.forename: Alessandro
authors.initials: A
authors.lastname: Cappelani
authors.forename: Salvatore
authors.initials: S
authors.lastname: Cuzzocrea
mesh_terms: D000818:Animals; D017304:Annexin A5 / Q000378:metabolism; D053222:Fas Ligand Protein / Q000378:metabolism; D020287:In Situ Nick-End Labeling / Q000379:methods; D016753:Interleukin-10 / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D053583:Interleukin-1beta / Q000378:metabolism; D007796:Laminectomy / Q000379:methods; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009187:Myelitis / Q000209:etiology*; D009414:Nerve Growth Factors / Q000378:metabolism; D009504:Neutrophils / Q000502:physiology; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D009195:Peroxidase / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D011897:Random Allocation; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins / Q000378:metabolism; D013117:Spinal Cord Compression / Q000150:complications*; D013119:Spinal Cord Injuries / Q000209:etiology* / Q000473:pathology; D018709:Statistics, Nonparametric; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D017304:Annexin A5; D053222:Fas Ligand Protein; D053583:Interleukin-1beta; D009414:Nerve Growth Factors; D019253:Proto-Oncogene Proteins c-bcl-2; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins; D014409:Tumor Necrosis Factor-alpha; D051028:bcl-2-Associated X Protein; D016753:Interleukin-10; D009195:Peroxidase; D052247:Nitric Oxide Synthase Type II