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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4 Pt 1
pubmed:dateCreated
1999-6-15
pubmed:abstractText
Hypoxia-ischemia induces an inflammatory response in the immature central nervous system that may be important for development of brain injury. Recent data implicate that chemoattractant cytokines, chemokines, are involved in the recruitment of immune cells. The aim was to study alpha- and beta-chemokines in relation to the temporal activation of inflammatory cells after hypoxia-ischemia in immature rats. Hypoxia-ischemia was induced in 7-day-old rats (left carotid artery occlusion + 7.7% oxygen). The pups were decapitated at different times after the insult. Immunohistochemistry was used for evaluation of the inflammatory cell response and RT-PCR to analyze the cytokine mRNA and chemokine mRNA expression. A distinct interleukin-1beta and tumor necrosis factor-alpha cytokine expression was found 0-24 h after hypoxia-ischemia that was accompanied by induction of alpha-chemokines (growth related gene and macrophage inflammatory protein-2). In the next phase, the beta2-integrin expression was increased (12 h and onward) and neutrophils transiently invaded the vessels and tissue in the infarct region. The mRNA induction for the beta-chemokines macrophage inflammatory protein-1alpha, macrophage inflammatory protein-1beta, and RANTES preceded the expression of markers for lymphocytes [cluster of differentiation (CD)4, CD8], microglia/macrophages (MHC I), and natural killer cells in the infarct area. The activation of microglia/macrophages, CD4 lymphocytes, and astroglia persisted up to at least 42 d of postnatal age implicating a chronic component of immunoinflammatory activation. The expression of mRNA for alpha- and beta-chemokines preceded the appearance of immune cells suggesting that these molecules may have a role in the inflammatory response to insults in the immature central nervous system.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0031-3998
pubmed:author
pubmed:issnType
Print
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
500-9
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:10203141-Animals, pubmed-meshheading:10203141-Animals, Newborn, pubmed-meshheading:10203141-Brain, pubmed-meshheading:10203141-Brain Ischemia, pubmed-meshheading:10203141-CD4-Positive T-Lymphocytes, pubmed-meshheading:10203141-CD8-Positive T-Lymphocytes, pubmed-meshheading:10203141-Cerebral Infarction, pubmed-meshheading:10203141-Chemokine CCL5, pubmed-meshheading:10203141-Chemokines, pubmed-meshheading:10203141-Cytokines, pubmed-meshheading:10203141-Female, pubmed-meshheading:10203141-Gene Expression Regulation, pubmed-meshheading:10203141-Hypoxia, Brain, pubmed-meshheading:10203141-Ischemic Attack, Transient, pubmed-meshheading:10203141-Lymphocyte Activation, pubmed-meshheading:10203141-Macrophages, pubmed-meshheading:10203141-Male, pubmed-meshheading:10203141-Microglia, pubmed-meshheading:10203141-RNA, Messenger, pubmed-meshheading:10203141-Rats, pubmed-meshheading:10203141-Rats, Wistar, pubmed-meshheading:10203141-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:10203141-Transcription, Genetic
pubmed:year
1999
pubmed:articleTitle
Chemokine and inflammatory cell response to hypoxia-ischemia in immature rats.
pubmed:affiliation
Perinatal Center, Department of Physiology and Pharmacology, Göteborg University, Sweden.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't