Sema Uysal
Posters-Accepted Abstracts: J Neurol Disord
Multiple sclerosis (MS) is a common, autoimmune inflammatory disorder of the central nervous system (CNS) characterized by demyelination and succeeding axonal degeneration. The remission and recurrent relapsing disease affects young adults especially women. The cause of MS remains unclear; however, its pathogenesis involves a complex mechanism in the immune system, genetic and environmental factors. Inflammation of CNS plays a major role in the pathogenesis of MS. The trigger of the inflammation is unknown, but several studies have suggested that genetic, environmental, or infectious agents may influence development of the disease. Procalcitonin (PCT) is known as an important marker for sepsis. Moreover, PCT levels increased in patients with autoimmune disorders reflects systemic infection. According to recent reports the higher concentration of CRP is associated with MS. The proinflammatory cytokines such as interleukin-1 (IL-1), IL-6, tumor necrosis factor-α (TNF-α), interferons, macrophage migration inhibitory factor, HMGB1 (high mobility group B1) contribute to inflammation and neuronal damage via increased secretion of reactive oxygen species, including nitric oxide in MS. The higher levels of interferon-γ (IFN-γ), TNF-α, interleukins (ILs)-1β, 2, 4, 10, 13 have been shown in patients with MS. The glycoprotein YKL-40 (chitinase 3-like 1) synthesized by macrophages, neutrophil granulocytes, chondrocytes, synovial cells, bone cells, vascular smooth muscle cells, hepatocytes, mammary epithelial cells and other tissues. Although the function of YKL-40 is not fully understood, it is induced in inflamed tissues during inflammatory process. In addition, YKL-40 reflects neuroinflammation in acute and chronic neurological diseases such as MS, ALS, Alzheimerâ??s disease and different stages of brain infarction. The primary aim of this study was evaluation of the role of inflammation, specifically of PCT, YKL-40 and some cytokines in subjects with MS.
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