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Background  The human-specific, Gram-negative bacterium  Neisseria meningitidis  ( Nm ) is a leading cause of bacterial meningitis worldwide. The blood-cerebrospinal fluid barrier (BCSFB), which is constituted by the epithelial cells of the choroid plexus (CP), has been suggested as one of the potential entry sites of  Nm  into the CSF and can contribute to the inflammatory response during infectious diseases of the brain. Toll-like receptors (TLRs) are involved in mediating signal transduction caused by the pathogens.    Methods  Using a recently established  in vitro  model of the human BCSFB based on human malignant CP papilloma (HIBCPP) cells we investigated the cellular response of HIBCPP cells challenged with the meningitis-causing  Nm  strain, MC58, employing transcriptome and RT-PCR analysis, cytokine bead array, and enzyme-linked immunosorbent assay (ELISA). In comparison, we analyzed the answer to the closely related unencapsulated carrier isolate  Nm  α14. The presence of TLRs in HIBCPP and their role during signal transduction caused by  Nm  was studied by RT-PCR and the use of specific agonists and mutant bacteria.    Results  We observed a stronger transcriptional response after infection with strain MC58, in particular with its capsule-deficient mutant MC58siaD − , which correlated with bacterial invasion levels. Expression evaluation and Gene Set Enrichment Analysis pointed to a NFκB-mediated pro-inflammatory immune response involving up-regulation of the transcription factor IκBζ. Infected cells secreted significant levels of pro-inflammatory chemokines and cytokines, including, among others, IL8, CXCL1-3, and the IκBζ target gene product IL6. The expression profile of pattern recognition receptors in HIBCPP cells and the response to specific agonists indicates that TLR2/TLR6, rather than TLR4 or TLR2/TLR1, is involved in the cellular reaction following  Nm  infection.    Conclusions  Our data show that  Nm  can initiate a pro-inflammatory response in human CP epithelial cells probably involving TLR2/TLR6 signaling and the transcriptional regulator IκBζ.    Electronic supplementary material  The online version of this article (doi:10.1186/s12974-014-0163-x) contains supplementary material, which is available to authorized users.

Neisseria meningitidiselicits a pro-inflammatory response involving IκBζ in a human blood-cerebrospinal fluid barrier model