Expression Analysis of the Early Chemokine Response 4 h After in Vitro Traumatic Brain Injury

Overview

Journal Inflamm Res

Specialties Allergy & Immunology
Pathology

Date 2010 Nov 25

PMID 21104293

Citations 12

Authors

Astrid V Fahlenkamp

Mark Coburn

Michael Czaplik

Yu-Mi Ryang

Markus Kipp

Rolf Rossaint

Cordian Beyer

Affiliations

Soon will be listed here.

Abstract

Objective And Design: The importance of cytokine- and chemokine-mediated neuroinflammation in the progress of brain injury is becoming increasingly evident. We investigated the early local cytokine and chemokine expression and the development of tissue injury after moderate mechanical hippocampus trauma.

Material Or Subjects: Mouse organotypic hippocampal slice cultures.

Treatment: Drop-weight trauma in the CA1 region of the hippocampus.

Methods: Staining of necrotic tissue, PCR array and evaluation, real-time PCR, statistical analysis with a two-tailed, independent t test.

Results: At 12 and 24 h after trauma, the tissue injury spread from the primary mechanical lesion to the entire hippocampal formation. A pronounced up-regulation of distinct chemokine transcripts was found 4 h after in vitro traumatic brain injury which preceded the development of the secondary injury.

Conclusions: The enhanced expression of inflammatory genes might contribute to the development of the secondary trauma and could pinpoint future neuroinflammatory and neuroprotective targets for research and treatment.

Citing Articles

The Role of Nanotechnology in Understanding the Pathophysiology of Traumatic Brain Injury.

Selvaraj S, Weerasinghe L Cent Nerv Syst Agents Med Chem. 2024; 25(1):20-38.

PMID: 38676493 DOI: 10.2174/0118715249291999240418112531.

Neutrophils in traumatic brain injury (TBI): friend or foe?.

Liu Y, Li S, Dai S J Neuroinflammation. 2018; 15(1):146.

PMID: 29776443 PMC: 5960133. DOI: 10.1186/s12974-018-1173-x.

Acute death of astrocytes in blast-exposed rat organotypic hippocampal slice cultures.

Miller A, Shah A, Aperi B, Kurpad S, Stemper B, Glavaski-Joksimovic A PLoS One. 2017; 12(3):e0173167.

PMID: 28264063 PMC: 5338800. DOI: 10.1371/journal.pone.0173167.

Loss of PAFR prevents neuroinflammation and brain dysfunction after traumatic brain injury.

Yin X, Chen Z, Zhu X, Hu J Sci Rep. 2017; 7:40614.

PMID: 28094295 PMC: 5240097. DOI: 10.1038/srep40614.

Analysis of the Role of CX3CL1 (Fractalkine) and Its Receptor CX3CR1 in Traumatic Brain and Spinal Cord Injury: Insight into Recent Advances in Actions of Neurochemokine Agents.

Poniatowski L, Wojdasiewicz P, Krawczyk M, Szukiewicz D, Gasik R, Kubaszewski L Mol Neurobiol. 2016; 54(3):2167-2188.

PMID: 26927660 PMC: 5355526. DOI: 10.1007/s12035-016-9787-4.

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