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

• Published in: Journal of neuroinflammation Vol. 3; no. 1; p. 22
• Main Authors: Canova, Cecile, Neal, Jim W, Gasque, Philippe
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 02.09.2006; BioMed Central; BMC
• ISSN: 1742-2094; 1742-2094
• DOI: 10.1186/1742-2094-3-22

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. 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. 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. 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.