title: Proinflammatory cytokines in injured rat brain following perinatal asphyxia.
abstract: In contrast to astrogliosis, which is common to injuries of the adult CNS, in the developing brain this process is minimal. Reasons postulated for this include the relative immaturity of the immune system and the consequent insufficient production of cytokines to evoke astrogliosis. To explore this hypothesis, the study was undertaken to detect the presence of some proinflammatory cytokines in the injured rat brain following perinatal asphyxia (ischaemia/hypoxia). The localisation of TNF-alpha, IL-15, IL-17 and IL-17 receptors was visualised by means of immunohistochemistry. In numerous neurones of the rat brain, the IL-17 appeared to be constitutively expressed. In the early period of inflammation the IL-15 was produced mainly by the blood cells penetrating the injured brain but later it was synthesised also by reactive astrocytes surrounding brain cysts and forming dense astrogliosis around necrotic brain regions. The direct effect on astrogliosis of other estimated cytokines seems to be negligible. All the results lead to the conclusion that from all cytokines identified in the injured immature rat brain the IL-15 plays the most important role during inflammatory response and participates in the gliosis of reactive astrocytes.
authors.affiliation: Department of Developmental Neuropathology, Medical Research Centre, Polish Academy of Sciences, Warszawa, Poland. Maslinskad@cmdik.pan.pl
authors.forename: Danuta
authors.initials: D
authors.lastname: Maślińska
authors.forename: Milena
authors.initials: M
authors.lastname: Laure-Kamionowska
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Kaliszek
authors.forename: Dorota
authors.initials: D
authors.lastname: Makarewicz
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001253:Astrocytes / Q000378:metabolism / Q000473:pathology; D001921:Brain / Q000254:growth & development / Q000276:immunology* / Q000378:metabolism / Q000473:pathology*; D002545:Brain Ischemia / Q000276:immunology* / Q000378:metabolism / Q000473:pathology*; D016207:Cytokines / Q000378:metabolism*; D007839:Functional Laterality; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000209:etiology / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D007150:Immunohistochemistry; D019409:Interleukin-15 / Q000378:metabolism; D020381:Interleukin-17 / Q000378:metabolism; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D018121:Receptors, Cytokine / Q000378:metabolism; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D016207:Cytokines; D005904:Glial Fibrillary Acidic Protein; D019409:Interleukin-15; D020381:Interleukin-17; D018121:Receptors, Cytokine; D014409:Tumor Necrosis Factor-alpha