Skip to main content

Advertisement

Log in

Inflammation of the Choroid Plexus and Ependymal Layer of the Ventricle Following Intraventricular Hemorrhage

  • Brief Communications
  • Published:
Translational Stroke Research Aims and scope Submit manuscript

Abstract

Intraventricular hemorrhage (IVH), which afflicts thousands of people of all ages every year, frequently results in the development of communicating hydrocephalus. Classically, IVH-induced hydrocephalus has been attributed to reduced resorption of cerebrospinal fluid (CSF) due to dysfunction of arachnoid granulations, but this explanation may be incomplete. We hypothesized that IVH would cause inflammation of the choroid plexus and of the ependymal lining of the ventricles, resulting in dysfunction of these barrier cells. Barrier dysfunction, in turn, would be expected to cause an increase in production of abnormal protein-rich CSF and transependymal migration of CSF. We tested this hypothesis using a rat model of IVH, in which 160 μl of autologous blood was infused into the lateral ventricle, resulting in a twofold increase in ventricular size 48 h later. In this model, we found significant activation of nuclear factor κB (NF-κB) signaling by the CSF barrier cells of the choroid plexus and ependymal lining. Moreover, these inflammatory changes were associated with abnormal uptake of serum-derived IgG by the barrier cells, a phenomenon closely linked to abnormal permeability of the blood–brain barrier. We conclude that inflammation marked by NF-κB signaling is a prominent feature after IVH and may account for certain pathophysiological sequelae associated with IVH.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Fig. 1
Fig. 2
Fig. 3

References

  1. Engelhardt B, Sorokin L. The blood–brain and the blood–cerebrospinal fluid barriers: function and dysfunction. Semin Immunopathol. 2009;31:497–511.

    Article  PubMed  Google Scholar 

  2. Hanley DF. Intraventricular hemorrhage: severity factor and treatment target in spontaneous intracerebral hemorrhage. Stroke. 2009;40:1533–8.

    Article  PubMed  Google Scholar 

  3. Hudgins RJ. Posthemorrhagic hydrocephalus of infancy. Neurosurg Clin N Am. 2001;12:743–51.

    PubMed  CAS  Google Scholar 

  4. Johansson PA, Dziegielewska KM, Liddelow SA, et al. The blood–CSF barrier explained: when development is not immaturity. Bioessays. 2008;30:237–48.

    Article  PubMed  CAS  Google Scholar 

  5. Jordan LC, Kleinman JT, Hillis AE. Intracerebral hemorrhage volume predicts poor neurologic outcome in children. Stroke. 2009;40:1666–71.

    Article  PubMed  Google Scholar 

  6. Lodhia KR, Shakui P, Keep RF. Hydrocephalus in a rat model of intraventricular hemorrhage. Acta Neurochir Suppl. 2006;96:207–11.

    Article  PubMed  CAS  Google Scholar 

  7. Matsumura K, Matsuda M, Handa J, et al. Magnetic resonance imaging with aneurysmal subarachnoid hemorrhage: comparison with computed tomography scan. Surg Neurol. 1990;34:71–8.

    Article  PubMed  CAS  Google Scholar 

  8. Simard JM, Geng Z, Woo SK, et al. Glibenclamide reduces inflammation, vasogenic edema, and caspase-3 activation after subarachnoid hemorrhage. J Cereb Blood Flow Metab. 2009;29:317–30.

    Article  PubMed  CAS  Google Scholar 

  9. Simard JM, Yurovsky V, Tsymbalyuk N, et al. Protective effect of delayed treatment with low-dose glibenclamide in three models of ischemic stroke. Stroke. 2009;40:604–9.

    Article  PubMed  CAS  Google Scholar 

  10. Wolburg H, Paulus W. Choroid plexus: biology and pathology. Acta Neuropathol. 2010;119:75–88.

    Article  PubMed  Google Scholar 

Download references

Acknowledgements

This work was supported by grants to JMS from the National Heart, Lung and Blood Institute (HL082517) and the National Institute of Neurological Disorders and Stroke (NS061808, NS060801).

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to J. Marc Simard.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Simard, P.F., Tosun, C., Melnichenko, L. et al. Inflammation of the Choroid Plexus and Ependymal Layer of the Ventricle Following Intraventricular Hemorrhage. Transl. Stroke Res. 2, 227–231 (2011). https://doi.org/10.1007/s12975-011-0070-8

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s12975-011-0070-8

Keywords

Navigation