Research

Expression of innate immune complement regulators on brain epithelial cells during human bacterial meningitis

Cecile Canova¹ , Jim W Neal² and Philippe Gasque^1,3

¹  Brain Inflammation and Immunity Group, Department of Medical Biochemistry, Cardiff University, Heath Park, Cardiff, CF14 4XN, UK

²  Department of Pathology, Neuropathology Laboratory; Cardiff University, Heath Park, Cardiff, CF14 4XN, UK

³  LBGM, Faculty of Sciences and Technologies, University of la Reunion, 15 Avenue René Cassin, BP7151, 97715, Saint Denis, Reunion

author email corresponding author email

Journal of Neuroinflammation 2006, 3:22doi:10.1186/1742-2094-3-22

Published:	2 September 2006

Abstract

Background

In meningitis, the cerebrospinal fluid contains high levels of innate immune molecules (e.g. complement) which are essential to ward off the infectious challenge and to promote the infiltration of phagocytes (neutrophils, monocytes). However, epithelial cells of either the ependymal layer, one of the established niche for adult neural stem cells, or of the choroid plexus may be extremely vulnerable to bystander attack by cytotoxic and cytolytic complement components.

Methods

In this study, we assessed the capacity of brain epithelial cells to express membrane-bound complement regulators (ie, CD35, CD46, CD55 and CD59) in vitro and in situ by immunostaining of control and meningitis human brain tissue sections.

Results

Double immunofluorescence experiments for ependymal cell markers (GFAP, S100, ZO-1, E-cadherin) and complement regulators indicated that the human ependymal cell line model was strongly positive for CD55, CD59 compared to weak stainings for CD46 and CD35. In tissues, we found that CD55 was weakly expressed in control choroid plexus and ependyma but was abundantly expressed in meningitis. Anti-CD59 stained both epithelia in apical location while increased CD59 staining was solely demonstrated in inflamed choroid plexus. CD46 and CD35 were not detected in control tissue sections. Conversely, in meningitis, the ependyma, subependyma and choroid plexus epithelia were strongly stained for CD46 and CD35.

Conclusion

This study delineates for the first time the capacity of brain ependymal and epithelial cells to respond to and possibly sustain the innate complement-mediated inflammatory insult.