Selective chemokine mRNA expression following brain injury

Hausmann, Elda H.S.; Berman, Nancy E.J.; Wang, Yuying; Meara, J.Brad; Wood, Gary W.; Klein, Robert M.

doi:10.1016/s0006-8993(97)01160-8

Cited by 110 publications

(62 citation statements)

References 52 publications

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“…After cryogenic lesion to the cerebral cortex MCP-1 mRNA expression peaked at 6 h, remained elevated for 24 h and then declined by 48 h. IP-10 expression was not upregulated in that brain injury model (Grzybicki et al, 1998). Compatible results were reported by Hausmann and colleagues, who found selective upregulation of MCP-1 expression after sterile but not LPS-augmented cerebral trauma (Hausmann et al, 1998).…”

Section: Chemokines In Nonimmunologic Cns Injurymentioning

confidence: 64%

“…Astrocytes, macrophages, endothelial cells, microglia Glabinski et al, 1996;Berman et al, 1996;Ghirnikar et al, 1996;Hausmann et al, 1998;McTigue et al, 1998 Wang et al, 1995;Lu et al, 1993;Yamasaki et al, 1995;Kim et al, 1995;Takami et al, 1997;Gourmaia et al, 1997;Ivacko et al, 1997 have not been identi®ed so far. One of them is CXCR5 receptor isolated initially from Burkitt's lymphoma cells but expressed also in mature B cells and in brain neurons (Kaiser et al, 1993).…”

Section: Chemokine Receptors In Cns Pathologymentioning

confidence: 99%

See 1 more Smart Citation

Chemokines and chemokine receptors in CNS pathology

Głąbiński¹,

Ransohoff²

1999

J Neurovirol

170

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Section: Chemokines In Nonimmunologic Cns Injurymentioning

confidence: 64%

Section: Chemokine Receptors In Cns Pathologymentioning

confidence: 99%

Chemokines and chemokine receptors in CNS pathology

Głąbiński¹,

Ransohoff²

1999

J Neurovirol

170

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“…These initial events fuel further release of inflammatory mediators which facilitate influx of extracerebral inflammatory cells by vascular endothelial changes and chemotaxis. Studies have also shown the role of adhesion molecules such as vascular cell adhesion molecule, P-selectin, intracellular adhesion molecule-1 and gradient of chemotactic chemokines in upregulating these events (Hausmann et al, 1998). The ensuing extracellular oedema is triggered by vascular dilatation and leakage as a result of vasoactive inflammatory molecules such as nitric oxide (NO) and vascular endothelial growth factor, as well as activations of complement system by dying cells to aggravate the initial inflammation and secondary tissue damage (Grzybicki et al, 1998;Stahel et al, 1998).…”

Section: Ultramicroscopic Eventsmentioning

confidence: 99%

Neurointensive Care Monitoring for Severe Traumatic Brain Injury

Idris¹,

Mustapha²,

Abdullah³

2012

Brain Injury - Pathogenesis, Monitoring, Recovery and Management

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“…Using the ependymal route, described by Martino et al (26), allows vectors to distribute throughout cerebrospinal fluid (CSF) and infect ependymal and leptomeningeal cells, which in turn secrete the product of the transgene into the CSF. This route avoids the traumatic effects of tissue injury associated with intraparenchymal and intracerebroventricular injections, which can include chemokine production and disruption of the blood-brain barrier (27)(28)(29)(30).…”

Section: Ifn-␥-induced Chemokines Synergize With Pertussis Toxin To Pmentioning

confidence: 99%

IFN-γ-Induced Chemokines Synergize with Pertussis Toxin to Promote T Cell Entry to the Central Nervous System

Millward

Caruso

Campbell

et al. 2007

The Journal of Immunology

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Inflammation of the CNS, which occurs during multiple sclerosis and experimental autoimmune encephalomyelitis, is characterized by increased levels of IFN-γ, a cytokine not normally expressed in the CNS. To investigate the role of IFN-γ in CNS, we used intrathecal injection of a replication-defective adenovirus encoding murine IFN-γ (AdIFNγ) to IFN-γ-deficient (GKO) mice. This method resulted in stable, long-lived expression of IFN-γ that could be detected in cerebrospinal fluid using ELISA and Luminex bead immunoassay. IFN-γ induced expression in the CNS of message and protein for the chemokines CXCL10 and CCL5, to levels comparable to those seen during experimental autoimmune encephalomyelitis. Other chemokines (CXCL2, CCL2, CCL3) were not induced. Mice lacking the IFN-γR showed no response, and a control viral vector did not induce chemokine expression. Chemokine expression was predominantly localized to meningeal and ependymal cells, and was also seen in astrocytes and microglia. IFN-γ-induced chemokine expression did not lead to inflammation. However, when pertussis toxin was given i.p. to mice infected with the IFN-γ vector, there was a dramatic increase in the number of T lymphocytes detected in the CNS by flow cytometry. This increase in blood-derived immune cells in the CNS did not occur with pertussis toxin alone, and did not manifest as histologically detectable inflammatory pathology. These results show that IFN-γ induces a characteristic glial chemokine response that by itself is insufficient to promote inflammation, and that IFN-γ-induced CNS chemoattractant signals can synergize with a peripheral infectious stimulus to drive T cell entry into the CNS.

show abstract

Selective chemokine mRNA expression following brain injury

Cited by 110 publications

References 52 publications

Chemokines and chemokine receptors in CNS pathology

Chemokines and chemokine receptors in CNS pathology

Neurointensive Care Monitoring for Severe Traumatic Brain Injury

IFN-γ-Induced Chemokines Synergize with Pertussis Toxin to Promote T Cell Entry to the Central Nervous System

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