Complement C3 and C5 play critical roles in traumatic brain cryoinjury: blocking effects on neutrophil extravasation by C5a receptor antagonist

Sewell, Diane; Nacewicz, Brendon M.; Liu, Frances; Macvilay, Sinarack; Erdei, Anna; Lambris, John D.; Sándor, Mátyás; Fábry, Zsuzsa

doi:10.1016/j.jneuroim.2004.06.003

Cited by 123 publications

(115 citation statements)

References 44 publications

(34 reference statements)

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“…As previously shown (20), cryo-injury to the brain disrupted the blood brain barrier immediately after insult, which induced brain edema followed by reactive gliosis in the present experimental model. In an intact region, testican-1 mRNA was clearly detected in hippocampal pyramidal neurons (Fig.…”

Section: Resultssupporting

confidence: 73%

Altered expression pattern of testican-1 mRNA after brain injury

et al. 2011

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Testican, a chondroitin/heparan sulfate proteoglycan, is primarily expressed in neurons of the adult and embryonic mouse brain, suggesting its role in normal and/or proliferation and differentiation processes of neurons. However, the role of testican in injured brain remains unclear. In the present study we investigated testican-1 mRNA expression pattern after cryo-injury of the brain. In situ hybridization histochemistry revealed that testican-1 mRNA is induced in the region surrounding the necrotic tissue. Time course study of testican-1 mRNA showed the highest level of signal intensity at 7 days after the injury. To determine which cell types express testican-1 mRNA, we performed in situ hybridization histochemistry combined with immunohistochemistry of several cell markers. Testican-1 mRNA signals were detected in the proximal reactive astrocytes, whereas the distribution pattern of testican-1 mRNA positive cells was different from those of mature oligodendrocytes and activated microglia. In addition, signals for testican-1 mRNA overlapped with those of FGF-2 mRNA, showing that these molecules are coexpressed in reactive astrocytes. These results suggest a possibility that testican-1 plays a permissive role for regenerating axons in reactive astrocytes after injury.

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Section: Resultssupporting

confidence: 73%

Altered expression pattern of testican-1 mRNA after brain injury

et al. 2011

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“…Cytofluorimetric analysis showed that ϳ95% of cells were CD8 ϩ V␣2 ϩ T cells (OVA-specific) and Ͻ0.5% of them were CD11c ϩ after the depletion (data not shown). Lymphocytes were also isolated from organotypic culture as described previously (12). Lymphocytes were isolated from the slices and/or the harvested culture medium.…”

Section: Lymphocyte Isolationmentioning

confidence: 99%

In Situ Activation of Antigen-Specific CD8+ T Cells in the Presence of Antigen in Organotypic Brain Slices

Ling

Verbny

Banks

et al. 2008

The Journal of Immunology

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The activation of Ag-specific T cells locally in the CNS could potentially contribute to the development of immune-mediated brain diseases. We addressed whether Ag-specific T cells could be stimulated in the CNS in the absence of peripheral lymphoid tissues by analyzing Ag-specific T cell responses in organotypic brain slice cultures. Organotypic brain slice cultures were established 1 h after intracerebral OVA Ag microinjection. We showed that when OVA-specific CD8+ T cells were added to Ag-containing brain slices, these cells became activated and migrated into the brain to the sites of their specific Ags. This activation of OVA-specific T cells was abrogated by the deletion of CD11c+ cells from the brain slices of the donor mice. These data suggest that brain-resident CD11c+ cells stimulate Ag-specific naive CD8+ T cells locally in the CNS and may contribute to immune responses in the brain.

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“…Sewell et al [35] recently demonstrated that mice deficient in complement factor C3 expressed significantly lower levels of inflammatory cytokines than did wild-type mice, and complement inhibition has been shown to attenuate CNS injury, whether induced by external agents or genetic deficiency [1,25,43].…”

Section: Introductionmentioning

confidence: 99%

Neurosteroids reduce inflammation after TBI through CD55 induction

VanLandingham

Cekić

Cutler

et al. 2007

Neuroscience Letters

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The inflammatory cascade that follows traumatic brain injury may lead to secondary cell death and can impede recovery of function. Complement factors and their convertases are increased in glia after brain injury and lead to the production of inflammatory products that kill vulnerable neurons. Progesterone and its metabolite allopregnanolone (5α-pregnan-3β-ol-20-one) have been shown to reduce the expression of inflammatory cytokines in the acute stages of brain injury, although how they do this is not completely understood. In this study we show that both progesterone and allopregnanolone treatments enhance the production of CD55 following contusion injuries of the cerebral cortex in rats. CD55, a single-chain type 1 cell surface protein, is a potent inhibitor of the complement convertases which are activators of the inflammatory cascade. The increased expression of CD55 could be an important mechanism by which steroids help to reduce the cerebral damage caused by inflammation.

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Complement C3 and C5 play critical roles in traumatic brain cryoinjury: blocking effects on neutrophil extravasation by C5a receptor antagonist

Cited by 123 publications

References 44 publications

Altered expression pattern of testican-1 mRNA after brain injury

Altered expression pattern of testican-1 mRNA after brain injury

In Situ Activation of Antigen-Specific CD8+ T Cells in the Presence of Antigen in Organotypic Brain Slices

Neurosteroids reduce inflammation after TBI through CD55 induction

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