title: Chronic systemic IL-1β exacerbates central neuroinflammation independently of the blood-brain barrier integrity.
abstract: Peripheral circulating cytokines are involved in immune to brain communication and systemic inflammation is considered a risk factor for flaring up the symptoms in most neurodegenerative diseases. We induced both central inflammatory demyelinating lesion, and systemic inflammation with an interleukin-1β expressing adenovector. The peripheral pro-inflammatory stimulus aggravated the ongoing central lesion independently of the blood-brain barrier (BBB) integrity. This model allows studying the role of specific molecules and cells (neutrophils) from the innate immune system, in the relationship between central and peripheral communication, and on relapsing episodes of demyelinating lesions, along with the role of BBB integrity.
authors.affiliation: Laboratorio de Terapias Regenerativas y Protectoras del Sistema Nervioso, Leloir Institute Foundation, Institute for Biochemical Investigations, CONICET, Buenos Aires, Argentina. Electronic address: vmurta.fmed@gmail.com.
authors.forename: Verónica
authors.initials: V
authors.lastname: Murta
authors.affiliation: Laboratorio de Terapias Regenerativas y Protectoras del Sistema Nervioso, Leloir Institute Foundation, Institute for Biochemical Investigations, CONICET, Buenos Aires, Argentina. Electronic address: mfarias@leloir.org.ar.
authors.forename: María Isabel
authors.initials: MI
authors.lastname: Farías
authors.affiliation: Laboratorio de Terapias Regenerativas y Protectoras del Sistema Nervioso, Leloir Institute Foundation, Institute for Biochemical Investigations, CONICET, Buenos Aires, Argentina. Electronic address: fpitossi@leloir.org.ar.
authors.forename: Fernando Juan
authors.initials: FJ
authors.lastname: Pitossi
authors.affiliation: Laboratorio de Terapias Regenerativas y Protectoras del Sistema Nervioso, Leloir Institute Foundation, Institute for Biochemical Investigations, CONICET, Buenos Aires, Argentina. Electronic address: carinaferrari@gmail.com.
authors.forename: Carina Cintia
authors.initials: CC
authors.lastname: Ferrari
mesh_terms: D000256:Adenoviridae / Q000502:physiology; D000818:Animals; D001812:Blood-Brain Barrier / Q000187:drug effects / Q000503:physiopathology*; D002490:Central Nervous System / Q000378:metabolism / Q000473:pathology*; D016207:Cytokines / Q000235:genetics / Q000378:metabolism; D004333:Drug Administration Routes; D005786:Gene Expression Regulation; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D000949:Histocompatibility Antigens Class II / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000139:chemically induced* / Q000473:pathology*; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism* / Q000633:toxicity*; D007962:Leukocytes / Q000187:drug effects / Q000473:pathology; D008099:Liver / Q000187:drug effects; D008297:Male; D009504:Neutrophils / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors
chemical_list: D016207:Cytokines; D005904:Glial Fibrillary Acidic Protein; D000949:Histocompatibility Antigens Class II; D053583:Interleukin-1beta
keywords: Blood–brain barrier; Interleukin-1β; Multiple sclerosis; Neuroinflammation; Neutrophils; Systemic inflammation