Transcriptomic profiling of choroid plexus in experimental autoimmune encephalomyelitis

Multiple sclerosis (MS) is a demyelinating disease causing major neurological disability in young adults. We characterized the transcriptome of the choroid plexus (CP), which is part of the blood-brain barriers and the major site of cerebrospinal fluid (CSF) production, in the experimental autoimmune encephalomyelitis mouse model of MS. Genes encoding for adhesion molecules, chemokines and cytokines displayed the most altered expression, supporting the CP as a site of immune-brain interaction in MS. The gene encoding for lipocalin 2 (LCN2) was the most up-regulated, and CSF LCN2 levels coincided with the phases of active disease. Total RNA was isolated with Trizol (Invitrogen, Carlsbad, CA, USA) following the manufacturer’s instructions. After quality assessment using the Agilent Bioanalyzer (Agilent Technologies, CA, USA), 100ng of total RNA from 3 pooled controls and 3 or 2 pooled samples of each experimental autoimmune encephalomyelitis (EAE) phase were amplified and labelled with the Illumina TotalPrep RNA Amplification Kit (Illumina Inc., San Diego, CA, USA). The labeled cRNA was then hybridized using the recommended protocol in a total of two Illumina Whole-Genome MouseRef-8 expression Beadchips (Illumina Inc., San Diego, CA, USA).