RGD Reference Report - Dynamics of neuroinflammation in the macrosphere model of arterio-arterial embolic focal ischemia: an approximation to human stroke patterns. - Rat Genome Database

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Dynamics of neuroinflammation in the macrosphere model of arterio-arterial embolic focal ischemia: an approximation to human stroke patterns.

Authors: Walberer, M  Dennin, MA  Simard, ML  Emig, B  Jander, S  Fink, GR  Schroeter, M 
Citation: Walberer M, etal., Exp Transl Stroke Med. 2010 Dec 20;2(1):22.
RGD ID: 4891154
Pubmed: PMID:21171972   (View Abstract at PubMed)
PMCID: PMC3024233   (View Article at PubMed Central)
DOI: DOI:10.1186/2040-7378-2-22   (Journal Full-text)

ABSTRACT: BACKGROUND: Neuroinflammation evolves as a multi-facetted response to focal cerebral ischemia. It involves activation of resident glia cell populations, recruitment of blood-derived leucocytes as well as humoral responses. Among these processes, phagocyte accumulation has been suggested to be a surrogate marker of neuroinflammation. We previously assessed phagocyte accumulation in human stroke by MRI. We hypothesize that phagocyte accumulation in the macrosphere model may resemble the temporal and spatial patterns observed in human stroke. METHODS: In a rat model of permanent focal ischemia by embolisation of TiO2-spheres we assessed key features of post-ischemic neuroinflammation by the means of histology, immunocytochemistry of glial activation and influx of hematogeneous cells, and quantitative PCR of TNF-a, IL-1, IL-18, and iNOS mRNA. RESULTS: In the boundary zone of the infarct, a transition of ramified microglia into ameboid phagocytic microglia was accompanied by an up-regulation of MHC class II on the cells after 3 days. By day 7, a hypercellular infiltrate consisting of activated microglia and phagocytic cells formed a thick rim around the ischemic infarct core. Interestingly, in the ischemic core microglia could only be observed at day 7. TNF-alpha was induced rapidly within hours, IL-1beta and iNOS peaked within days, and IL-18 later at around 1 week after ischemia. CONCLUSIONS: The macrosphere model closely resembles the characteristical dynamics of postischemic inflammation previously observed in human stroke. We therefore suggest that the macrosphere model is highly appropriate for studying the pathophysiology of stroke in a translational approach from rodent to human.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Stroke  ISOIl18 (Rattus norvegicus)4891154; 4891154mRNA:increased expression:brainRGD 
Stroke  IEP 4891154; 4891154; 4891154mRNA:increased expression:brainRGD 
Stroke  ISONos2 (Rattus norvegicus)4891154; 4891154mRNA:increased expression:brainRGD 
Stroke  ISOTnf (Rattus norvegicus)4891154; 4891154mRNA:increased expression:brainRGD 

Objects Annotated

Genes (Rattus norvegicus)
Il18  (interleukin 18)
Nos2  (nitric oxide synthase 2)
Tnf  (tumor necrosis factor)

Genes (Mus musculus)
Il18  (interleukin 18)
Nos2  (nitric oxide synthase 2, inducible)
Tnf  (tumor necrosis factor)

Genes (Homo sapiens)
IL18  (interleukin 18)
NOS2  (nitric oxide synthase 2)
TNF  (tumor necrosis factor)


Additional Information