Peripheral inflammatory stimulus exacerbates the ongoing central damage in an inflammatory model of demyelination

FERRARI, CC

Rio de janeiro

Congreso; First Meeting of the Institute of Glia; 2011

Brasilian Institute of Glia

The role of inflammation in the progression of neurodegenerative disease remains still obscure. In addition, peripheral inflammation can trigger the synthesis of cytokines in the CNS. Recent studies have revealed that a peripheral pro-inflammatory stimuli can exacerbate ongoing central damage. Peripheral pro-inflammatory stimuli can switch the microglia to an aggressive state inducing a more robust response in the CNS. Clinical and experimental studies of Parkinson`s disease (PD) and Alzheimer have demonstrated that peripheral infections worsen the symptoms of the disease. Our laboratory, has shown that a peripheral pro-inflammatory stimuli exacerbated the neurodegeneration in Parkinson’s Disease (PD). Clinical study has demonstrated that symptoms of EM are exacerbated in a temporal window close to a systemic infection. However, no studies in experimental models have been done until now.We have developed a model that long term expression of IL-1b induced neutrophil infiltration, blood brain barrier breakdown and reversible demyelination (Ferrari et al., 2004). Therefore, we have generated a model of relapsing/remitting MS to study in isolation the innate immune system components. I will talk about the pathology of peripheral inflammations on the demyelination and remyelination processes in a novel experimental model induced by the chronic expression of IL-1b in the Central Nervous System.