title: Interleukin-10 and interleukin-10 receptor-I are upregulated in glial cells after an excitotoxic injury to the postnatal rat brain.
abstract: Inflammation is an important determinant of the severity and outcome of central nervous system injury. The endogenous anti-inflammatory cytokine interleukin-10 (IL-10) is upregulated in the injured adult central nervous system where it controls and terminates inflammatory processes. The developing brain, however, displays differences in susceptibility to insults and in associated inflammatory responses from the adult brain; the anatomic and temporal patterns of injury-induced IL-10 expression in the immature brain after excitotoxic injury are unknown. We analyzed the spaciotemporal gene and protein expression of IL-10 and its receptor (IL-10RI) in N-methyl-d-aspartate-induced excitotoxic injury in 9-day-old and control rats using quantitative reverse transcriptase polymerase chain reaction, enzyme-linked immunosorbent assay, and immunohistochemistry. In noninjected control brains, both molecules were expressed mainly in white matter on glial cells and blood vessels; IL-10 was also observed on blood vessels in gray matter and in glial fibrillary acidic protein-positive processes in the hippocampus and near leptomeningeal and ventricle surfaces. In N-methyl-d-aspartate-injected brains, IL-10 gene and protein expression were maximal at 72 hours postinjection; IL-10RI gene and protein expression peaked at 48 hours postinjection. Interleukin-10 and IL-10RI expression in injured areas was mainly found in reactive astrocytes and in microglia/macrophages. The expression patterns of IL-10 and IL-10R suggest possible developmental roles, and their upregulation after injury suggests that this expression may have anti-inflammatory effects in distinct anatomic sites in the immature brain.
authors.affiliation: Medical Histology, Department of Cellular Biology, and Neuroscience Institute, Autonomous University of Barcelona, Barcelona, Spain. Pau.Gonzalez@uab.es
authors.forename: Pau
authors.initials: P
authors.lastname: Gonzalez
authors.forename: Ferran
authors.initials: F
authors.lastname: Burgaya
authors.forename: Laia
authors.initials: L
authors.lastname: Acarin
authors.forename: Hugo
authors.initials: H
authors.lastname: Peluffo
authors.forename: Bernardo
authors.initials: B
authors.lastname: Castellano
authors.forename: Berta
authors.initials: B
authors.lastname: Gonzalez
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001808:Blood Vessels / Q000187:drug effects / Q000378:metabolism; D001930:Brain Injuries / Q000139:chemically induced / Q000473:pathology* / Q000503:physiopathology; D053331:Ectodysplasins / Q000378:metabolism; D018690:Excitatory Amino Acid Agonists / Q000633:toxicity; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D016753:Interleukin-10 / Q000235:genetics / Q000378:metabolism*; D053709:Interleukin-10 Receptor alpha Subunit / Q000235:genetics / Q000378:metabolism*; D008297:Male; D016202:N-Methylaspartate / Q000633:toxicity; D009457:Neuroglia / Q000187:drug effects / Q000502:physiology*; D010751:Phosphopyruvate Hydratase / Q000378:metabolism; D037121:Plant Lectins / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D020318:Rats, Long-Evans; D013997:Time Factors; D015854:Up-Regulation / Q000187:drug effects / Q000502:physiology*
chemical_list: D053331:Ectodysplasins; D018690:Excitatory Amino Acid Agonists; D005904:Glial Fibrillary Acidic Protein; D053709:Interleukin-10 Receptor alpha Subunit; D037121:Plant Lectins; D012333:RNA, Messenger; C034981:tomato lectin; D016753:Interleukin-10; D016202:N-Methylaspartate; D010751:Phosphopyruvate Hydratase