Contributions
Abstract: EP1425
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - Immunology
Multiple Sclerosis (MS) is a demyelinating and inflammatory disease of the central nervous system (CNS) with an etiopathology to be elucidated. It is known that there is a direct involvement of the immune system and currently, there are more and more studies that put a special focus on the Oxidative Stress (OS) participation. OS involvement in MS has been described at CNS level; however the oxidative processes that explain this increase are still unknown. The aim of this work is to address the hypothesis that there is a direct involvement of mitochondrial and redox status of peripheral lymphocyte with the MS etiopathology. To this end, we present a cross-sectional, observational and comparative pilot study (n = 40) with two arms (EM = 20 and CTL = 20) matched for gender and age. The methodology used was flow cytometry to identify lymphocyte populations and quantitation of superoxide cation, immunoblotting for estimating mitochondrial complexes, commercial kits for detection of lactate and ABTS technique to estimate the plasma antioxidant capacity. In this work we described that lymphocytes from MS patients produced a significant increase in the production of superoxide (p = 0.031) compared to controls, this result could be due to decreased mitochondrial complex I, III and V (p = 0.032, 0.019 and 0.023, respectively) and responsible for increasing the lactate concentration (p = 0.005) and decreased plasma antioxidant capacity (p = 0.038) described in this work. This results suggests that part of the OS trigger widely reported at the level of CNS, could be a consequence of an impaired mitochondrial redox status in the peripheral lymphocytes of MS patients, deficiency that would be dragged to the CNS in the process of lymphocyte infiltration, increasing the production of free radicals that facilitate the oxidative imbalance and consequently the generation of OS described at CNS level.
Disclosure: Hugo Gonzalo: nothing to disclose
Abstract: EP1425
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - Immunology
Multiple Sclerosis (MS) is a demyelinating and inflammatory disease of the central nervous system (CNS) with an etiopathology to be elucidated. It is known that there is a direct involvement of the immune system and currently, there are more and more studies that put a special focus on the Oxidative Stress (OS) participation. OS involvement in MS has been described at CNS level; however the oxidative processes that explain this increase are still unknown. The aim of this work is to address the hypothesis that there is a direct involvement of mitochondrial and redox status of peripheral lymphocyte with the MS etiopathology. To this end, we present a cross-sectional, observational and comparative pilot study (n = 40) with two arms (EM = 20 and CTL = 20) matched for gender and age. The methodology used was flow cytometry to identify lymphocyte populations and quantitation of superoxide cation, immunoblotting for estimating mitochondrial complexes, commercial kits for detection of lactate and ABTS technique to estimate the plasma antioxidant capacity. In this work we described that lymphocytes from MS patients produced a significant increase in the production of superoxide (p = 0.031) compared to controls, this result could be due to decreased mitochondrial complex I, III and V (p = 0.032, 0.019 and 0.023, respectively) and responsible for increasing the lactate concentration (p = 0.005) and decreased plasma antioxidant capacity (p = 0.038) described in this work. This results suggests that part of the OS trigger widely reported at the level of CNS, could be a consequence of an impaired mitochondrial redox status in the peripheral lymphocytes of MS patients, deficiency that would be dragged to the CNS in the process of lymphocyte infiltration, increasing the production of free radicals that facilitate the oxidative imbalance and consequently the generation of OS described at CNS level.
Disclosure: Hugo Gonzalo: nothing to disclose