Background Experimental autoimmune encephalomyelitis rep resents a variety of animal models reflecting clinical and pathological characteristics of multiple sclerosis. MS is presumably a autoimmune CNS disease with stepwise or chronic progressive evolution of inflammation, demy elination, axonal injury and oligodendrocyte death selleck catalog inter twined with the nervous systems attempts to repair damage and regain homeostasis. The complexity of these processes remains a formidable obstacle to the elucida tion of the primary and driving pathogenetic events. Transcriptome studies of CNS tissue in MS and EAE prob ing many thousand gene products in parallel have resulted in interesting and unexpected target molecules possibly suitable Inhibitors,Modulators,Libraries for therapeutic trials in MS.

Most studies describing the transcriptional spinal cord profile in EAE have been performed in murine models. EAE induced by myelin oligodendrocyte protein in the rat represents a spectrum of diseases mimicking various forms of MS pathology depending on the selection of strain, gender and experimental Inhibitors,Modulators,Libraries procedures, respectively. In female Dark agouti rats, a chronic relapsing EAE variant can be induced, characterized by widespread demyelination, axonal damage and remyelination. MOG has been recognized as a particularly likely candi date for an initial antigen specific attack in the CNS dur ing MS, and T and B cell responses to MOG have been identified in MS patients and in EAE. This report presents for the first time spinal cord transcriptional data of a chronic EAE model in the rat.

We compared the mRNA expression profile of more than 26,000 transcripts in spinal cords of DA rats by a large scale gene expression approach using the DNA microarray technique. Expres sion profiling from spinal cord tissue comparing rats with EAE and healthy control rats was performed in three dis tinct stages Inhibitors,Modulators,Libraries of disease evolution, i. e. acute, recovery and relapsing phases of EAE. More than 1,100 significantly regulated Inhibitors,Modulators,Libraries transcripts were identified. While confirming well established features of EAE, we identified several dif ferentially upregulated transcripts not described previ ously. In more detail, we examined the secretory leukocyte protease inhibitor representing the most strongly upregulated gene in this study. SLPI is a homeostatic pro tein known to be expressed at mucosal surfaces by epithe lial cells, macrophages and neutrophils.

It is involved in the resolution of inflammation by suppressing protease activity, by attenuating innate immune responses and Inhibitors,Modulators,Libraries by selleck inhibiting the activation and proliferation of B cells. In the CNS its induction has been reported as a consequence of ischemic stroke and spinal cord injury. In this study we provide evidence that SLPI promotes oligodendroglial proliferation and differentia tion. We suggest that SLPI may have a novel and multiple roles in CNS inflammation, i. e.