Spatiotemporal Pattern of Neuroinflammation After Impact-Acceleration Closed Head Injury in the Rat
<p>Inflammatory processes have been implicated in the pathogenesis of traumatic brain damage. We analyzed the spatiotemporal expression pattern of the proinflammatory key molecules: interleukin-1<mml:math alttext="$eta$"> <mml:mi>β</mml:mi>...
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| Format: | Article |
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| Language: | English |
| Published: |
Wiley
2006-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://www.hindawi.com/GetArticle.aspx?doi=10.1155/MI/2006/90123 |
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| Summary: | <p>Inflammatory processes have been implicated in the pathogenesis of traumatic brain damage. We analyzed the spatiotemporal expression pattern of the proinflammatory key molecules: interleukin-1<mml:math alttext="$eta$"> <mml:mi>β</mml:mi> </mml:math>, interleukin-6, tumor necrosis factor-<mml:math alttext="$alpha$"> <mml:mi>α</mml:mi> </mml:math>, and inducible nitric oxide synthase in a rat closed head injury (CHI) paradigm. 51 rats were used for RT-PCR analysis after CHI, and 18 for immunocytochemistry. We found an early upregulation of IL-1<mml:math alttext="$eta$"> <mml:mi>β</mml:mi> </mml:math>, IL-6, and TNF-<mml:math alttext="$alpha$"> <mml:mi>α</mml:mi> </mml:math> mRNA between 1h and 7h after injury; the expression of iNOS mRNA only revealed a significant increase at 4h. After 24h, the expression decreased towards baseline levels, and remained low until 7d after injury. Immunocytochemically, IL-1<mml:math alttext="$eta$"> <mml:mi>β</mml:mi> </mml:math> induction was localized to ramified microglia in areas surrounding the primary impact place as well as deeper brain structures. Our study shows rapid induction of inflammatory gene expression that exceeds by far the primary impact site and might therefore contribute to tissue damage at remote sites.</p> |
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| ISSN: | 0962-9351 |