The alkaloid castanospermine is a potent inhibitor of oligosaccharide processing in vitro. Our recent findings indicating the importance of carbohydrate moieties in some critical step of the neuro-immunologic inflammatory process of allergic encephalomyelitis prompted us to investigate the effect of castanospermine on this disease process. The alkaloid inhibited passively induced allergic encephalomyelitis in a dose-dependent manner when administered continuously for 7 days beginning at the time of lymphocyte transfer. Although clinical disease was totally inhibited, treated animals did have inflammatory lesions in the central nervous system. These lesions were qualitatively different from those seen in untreated animals in that the inflammatory cells were tightly packed around the vessels and showed little migration into surrounding tissues. Castanospermine also effectively inhibited clinical disease in recipient animals which had had a previous episode of allergic encephalomyelitis. Castanospermine did not alter the disease when treatment was started after the onset of clinical symptoms.
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http://dx.doi.org/10.1016/0022-510x(89)90047-6 | DOI Listing |
Adv Sci (Weinh)
January 2025
Department of Neurology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
The dysfunction of stress granules (SGs) plays a crucial role in the pathogenesis of various neurological disorders, with T cell intracellular antigen 1 (TIA1) being a key component of SGs. However, the role and mechanism of TIA1-mediated SGs in experimental autoimmune encephalomyelitis (EAE) remain unclear. In this study, upregulation of TIA1, its translocation from the nucleus to the cytoplasm, and co-localization with G3BP1 (a marker of SGs) are observed in the spinal cord neurons of EAE mice.
View Article and Find Full Text PDFInt J Clin Exp Pathol
December 2024
Department of Experimental Medicine, King Abdullah International Medical Research Center (KAIMRC), King Saud Bin Abdulaziz University for Health Sciences (KSAU-HS), Ministry of National Guard-Health Affairs (MNGHA) Riyadh 11481, Saudi Arabia.
Background: Multiple sclerosis (MS) is a chronic, immune-mediated neurological disorder in which the immune system mistakenly attacks the myelin sheath, affecting the communication between the brain and the rest of the body.
Objective: This study investigated the prophylactic use of peptide inhibitor of trans-endothelial migration (PEPITEM), a novel peptide, in alleviating experimental autoimmune encephalomyelitis (EAE), a mouse model for Multiple Sclerosis (MS).
Methods: Female C57BL/6 female mice were assigned to the control, untreated EAE, or PEPITEM group.
Heliyon
January 2025
Department of Biochemistry and Molecular Biology, Life Science Faculty, Bangabandhu Sheikh Mujibur Rahman Science and Technology University, Gopalganj, 8100, Bangladesh.
Multiple Sclerosis (MS) is an autoimmune and chronic disease in the brain and spinal cord. MS has inflammatory progression characterized by its hallmark inflammatory plaques. The histological and clinical characteristics of MS are shared by Experimental Autoimmune Encephalomyelitis (EAE).
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Instituto de Biomedicina de Sevilla, IBiS/Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, 41013 Seville, Spain.
Multiple sclerosis (MS) is a neurodegenerative disease, with inflammation and oxidative stress in the central nervous system being the main triggers. There are many drugs that reduce the clinical signs of MS, but none of them cure the disease. Food proteins have been shown to contain encrypted peptides that can be released after hydrolysis and exert numerous biological activities.
View Article and Find Full Text PDFCell Rep
January 2025
Institute of Molecular Biology, Academia Sinica, Taipei, Taiwan. Electronic address:
Proteasomes generate antigenic peptides presented on cell surfaces-a process that, in neuroglia, is highly responsive to external stimuli. However, the function of the self-antigens presented by CNS parenchymal cells remains unclear. Here, we report that the fidelity of neuroglial self-antigens is crucial to suppress encephalitogenic T cell responses by elevating regulatory T (Treg) cell populations.
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