Bibliographies thématiques / Experimental Autoimmune Encephalomyelitis, Progesterone

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Littérature scientifique sur le sujet « Experimental Autoimmune Encephalomyelitis, Progesterone »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 10 mars 2023

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Articles de revues sur le sujet "Experimental Autoimmune Encephalomyelitis, Progesterone"

Giatti, S., D. Caruso, M. Boraso, F. Abbiati, E. Ballarini, D. Calabrese, M. Pesaresi et al. « Neuroprotective Effects of Progesterone in Chronic Experimental Autoimmune Encephalomyelitis ». Journal of Neuroendocrinology 24, n^o 6 (10 mai 2012) : 851–61. http://dx.doi.org/10.1111/j.1365-2826.2012.02284.x.

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Garay, Laura, Maria Claudia Gonzalez Deniselle, Regine Sitruk-Ware, Rachida Guennoun, Michael Schumacher et Alejandro F. De Nicola. « Efficacy of the selective progesterone receptor agonist Nestorone for chronic experimental autoimmune encephalomyelitis ». Journal of Neuroimmunology 276, n^o 1-2 (novembre 2014) : 89–97. http://dx.doi.org/10.1016/j.jneuroim.2014.08.619.

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Yates, M. A., Y. Li, P. Chlebeck, T. Proctor, A. A. Vandenbark et H. Offner. « Progesterone treatment reduces disease severity and increases IL-10 in experimental autoimmune encephalomyelitis ». Journal of Neuroimmunology 220, n^o 1-2 (mars 2010) : 136–39. http://dx.doi.org/10.1016/j.jneuroim.2010.01.013.

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Garay, L. I., M. C. González Deniselle, M. E. Brocca, A. Lima, P. Roig et A. F. De Nicola. « Progesterone down-regulates spinal cord inflammatory mediators and increases myelination in experimental autoimmune encephalomyelitis ». Neuroscience 226 (décembre 2012) : 40–50. http://dx.doi.org/10.1016/j.neuroscience.2012.09.032.

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Garay, Laura, Maria Claudia Gonzalez Deniselle, Maria Meyer, Juan José Lopez Costa, Analia Lima, Paulina Roig et Alejandro F. DeNicola. « Protective effects of progesterone administration on axonal pathology in mice with experimental autoimmune encephalomyelitis ». Brain Research 1283 (août 2009) : 177–85. http://dx.doi.org/10.1016/j.brainres.2009.04.057.

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Utevska, S. V. « Experimental autoimmune encephalomyelitis (EAE) course in prenatally stressed rat males, the offspring of mothers with different sensitivity to EAE ». Faktori eksperimental'noi evolucii organizmiv 24 (30 août 2019) : 244–48. http://dx.doi.org/10.7124/feeo.v24.1109.

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Aim. The research is aimed at investigating the effect of prenatal stress on the incidence and course of experimental autoimmune encephalomyelitis (EAE) as well as the level of sex hormones in 200-days-old male rats, offspring of females with different sensitivity to EAE induction. Methods. The incidence and severity of EAE including duration of latent period, duration of the period from the first to the maximum manifestation of motor disfunction, mean clinical scores, maximum level of motor disfunction (maximum clinical scores) were analyzed in rats with induced EAE. Serum testosterone, estradiol and progesterone levels were measure during Enzyme-Linked Immunosorbent Assay (ELISA). Results. The estradiol level of prenatally stressed males was significantly lower than in rats from the control group. Sensitive to EAE test male rats had lower testosterone levels than EAE resistant males, and the offspring of EAE sensitive mothers were more resistant to EAE induction than the offspring of EAE resistant mothers. Conclusions. Without significant changes in the course of EAE, the reduction in incidence depends on a combination of factors such as mother's sensitivity to EAE induction and prenatal stress. Keywords: experimental autoimmune encephalomyelitis (EAE), prenatal stress, sex hormones, sensitivity to EAE induction.

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Yu, Hong-jun, Jun Fei, Xing-shu Chen, Qi-yan Cai, Hong-liang Liu, Guo-dong Liu et Zhong-xiang Yao. « Progesterone attenuates neurological behavioral deficits of experimental autoimmune encephalomyelitis through remyelination with nucleus-sublocalized Olig1 protein ». Neuroscience Letters 476, n^o 1 (mai 2010) : 42–45. http://dx.doi.org/10.1016/j.neulet.2010.03.079.

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Ghoumari, Abdel Mouman, Charly Abi Ghanem, Narimène Asbelaoui, Michael Schumacher et Rashad Hussain. « Roles of Progesterone, Testosterone and Their Nuclear Receptors in Central Nervous System Myelination and Remyelination ». International Journal of Molecular Sciences 21, n^o 9 (30 avril 2020) : 3163. http://dx.doi.org/10.3390/ijms21093163.

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Progesterone and testosterone, beyond their roles as sex hormones, are neuroactive steroids, playing crucial regulatory functions within the nervous system. Among these, neuroprotection and myelin regeneration are important ones. The present review aims to discuss the stimulatory effects of progesterone and testosterone on the process of myelination and remyelination. These effects have been demonstrated in vitro (i.e., organotypic cultures) and in vivo (cuprizone- or lysolecithin-induced demyelination and experimental autoimmune encephalomyelitis (EAE)). Both steroids stimulate myelin formation and regeneration by acting through their respective intracellular receptors: progesterone receptors (PR) and androgen receptors (AR). Activation of these receptors results in multiple events involving direct transcription and translation, regulating general homeostasis, cell proliferation, differentiation, growth and myelination. It also ameliorates immune response as seen in the EAE model, resulting in a significant decrease in inflammation leading to a fast recovery. Although natural progesterone and testosterone have a therapeutic potential, their synthetic derivatives—the 19-norprogesterone (nestorone) and 7α-methyl-nortestosterone (MENT), already used as hormonal contraception or in postmenopausal hormone replacement therapies, may offer enhanced benefits for myelin repair. We summarize here a recent advancement in the field of myelin biology, to treat demyelinating disorders using the natural as well as synthetic analogs of progesterone and testosterone.

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Engler, Jan Broder, Nina Kursawe, María Emilia Solano, Kostas Patas, Sabine Wehrmann, Nina Heckmann, Fred Lühder et al. « Glucocorticoid receptor in T cells mediates protection from autoimmunity in pregnancy ». Proceedings of the National Academy of Sciences 114, n^o 2 (3 janvier 2017) : E181—E190. http://dx.doi.org/10.1073/pnas.1617115114.

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Pregnancy is one of the strongest inducers of immunological tolerance. Disease activity of many autoimmune diseases including multiple sclerosis (MS) is temporarily suppressed by pregnancy, but little is known about the underlying molecular mechanisms. Here, we investigated the endocrine regulation of conventional and regulatory T cells (Tregs) during reproduction. In vitro, we found the pregnancy hormone progesterone to robustly increase Treg frequencies via promiscuous binding to the glucocorticoid receptor (GR) in T cells. In vivo, T-cell–specific GR deletion in pregnant animals undergoing experimental autoimmune encephalomyelitis (EAE), the animal model of MS, resulted in a reduced Treg increase and a selective loss of pregnancy-induced protection, whereas reproductive success was unaffected. Our data imply that steroid hormones can shift the immunological balance in favor of Tregs via differential engagement of the GR in T cells. This newly defined mechanism confers protection from autoimmunity during pregnancy and represents a potential target for future therapy.

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Goudarzvand, Mahdi, Yaser Panahi, Reza Yazdani, Hosein Miladi, Saeed Tahmasebi, Amin Sherafat, Sanaz Afraei et al. « The Effects of D-aspartate on Neurosteroids, Neurosteroid Receptors, and Inflammatory Mediators in Experimental Autoimmune Encephalomyelitis ». Endocrine, Metabolic & ; Immune Disorders - Drug Targets 19, n^o 3 (15 avril 2019) : 316–25. http://dx.doi.org/10.2174/1871530318666181005093459.

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Objective: Experimental autoimmune encephalomyelitis (EAE) is a widely used model for multiple sclerosis. The present study has been designed to compare the efficiencies of oral and intraperitoneal (IP) administration of D-aspartate (D-Asp) on the onset and severity of EAE, the production of neurosteroids, and the expression of neurosteroid receptors and inflammatory mediators in the brain of EAE mice. Methods: In this study, EAE was induced in C57BL/6 mice treated with D-Asp orally (D-Asp-Oral) or by IP injection (D-Asp-IP). On the 20th day, brains (cerebrums) and cerebellums of mice were evaluated by histological analyses. The brains of mice were analyzed for: 1) Neurosteroid (Progesterone, Testosterone, 17β-estradiol) concentrations; 2) gene expressions of cytokines and neurosteroid receptors by reverse transcription polymerase chain reaction, and 3) quantitative determination of D-Asp using liquid chromatography-tandem mass spectrometry. Further, some inflammatory cytokines and matrix metalloproteinase-2 (MMP-2) were identified in the mouse serum using enzyme-linked immunosorbent assay kits. Results: Our findings demonstrated that after D-Asp was administered, it was taken up and accumulated within the brain. Further, IP injection of D-Asp had more beneficial effects on EAE severity than oral gavage. The concentration of the testosterone and 17β-estradiol in D-Asp-IP group was significantly higher than that of the control group. There were no significant differences in the gene expression of cytokine and neurosteroid receptors between control, D-Asp-IP, and D-Asp-Oral groups. However, IP treatment with D-Asp significantly reduced C-C motif chemokine ligand 2 and MMP-2 serum levels compared to control mice. Conclusion: IP injection of D-Asp had more beneficial effects on EAE severity, neurosteroid induction and reduction of inflammatory mediators than oral gavage.

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Thèses sur le sujet "Experimental Autoimmune Encephalomyelitis, Progesterone"

BALLARINI, ELISA. « Caratterizzazione di un modello di encefalomielite autoimmune sperimentale e ruolo neuroprotettivo del progesterone ». Doctoral thesis, Università degli Studi di Milano-Bicocca, 2012. http://hdl.handle.net/10281/39833.

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Studies concerning the role of neuroactive steroids in chronic models of Experimental Autoimmune Encephalomyelitis (EAE) are still scarce. First we considered different pathological targets in Dark Agouti (DA) rats affected by EAE in order to well characterize this chronic model of Multiple Sclerosis (MS) which well reflects the relapsing-remitting form of MS. We analyzed neuroinflammatory profile, assonopathy and neuroactive steroid levels in the spinal cord of DA rats affected by EAE. Data obtained at 14 dpi (i.e. days post induction) showed that acute neurological signs were associated with infiltrating T cells (CD3+) and macrophages (ED1+) and with microglial activation (MHC-II+ cells) which were accompanied by an increased expression of pro- and anti-inflammatory cytokines in the spinal cord. We immunolocalized a few damaged axons (SMI-32+) in the spinal cord white matter, moreover we identified a general decrease in the level of most neuroactive steroids analyzed. At 45 dpi we observed a decrease of inflammatory infiltration, of microglial cell activation and of cytokine gene expression respect to EAE rats at 14dpi. Assonopathy was exacerbated as demonstrated by the increase in SMI-32 immunoreactivity and by the decreased Na+,K+-ATPase activity. Changes in the neuroactive steroid level observed at 14dpi were maintained or reverted at 45dpi. Interestingly, the level of progesterone (PROG) significantly decreased only at 45dpi suggesting a possible role of this neuroactive steroid in the chronicization of EAE. Basing on this evidence, we performed a second study aimed to evaluate the possible neuroprotective properties of PROG treatment in DA rats affected by EAE. Data obtained at 45 dpi showed that PROG was able to improve EAE course by reducing the spinal cord neuroinflammation and microglia activation. Moreover PROG treatment was able to promote a functional recover of axons and to counteract the MBP protein reduction observed in EAE rats. Finally an increase in the levels of dihydroprogesterone and isopregnanolone (i.e. two PROG metabolites) was also observed in the spinal cord after PROG treatment providing evidence on PROG metabolic profile. Taken together these results indicate that PROG may have a role in the pathogenesis of EAE and that it is effective in reducing the severity of EAE in DA rats. Consequently our data may represent an interesting background for future treatments of MS based on synthetic analogous of PROG.

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Harness, Jacqueline. « Immunoregulation of experimental autoimmune encephalomyelitis / ». St. Lucia, Qld, 2002. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe17375.pdf.

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Isaksson, Magnus. « Initiation of Autoimmunity in Experimental Autoimmune Encephalomyelitis ». Doctoral thesis, Uppsala universitet, Molekylär medicin, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-173427.

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The events that trigger an autoimmune disease remain largely unknown. To study these events animal models are necessary because symptoms of autoimmune diseases are preceded by a long asymptomatic period in humans. Experimental autoimmune encephalomyelitis (EAE) is the best characterized model for cell mediated autoimmunity and an animal model for the human disease multiple sclerosis. EAE is induced in rodents by immunization with myelin antigens (Ags) together with adjuvants. After immunization, T cells are primed in the periphery by Ag presenting cells and subsequently invade the central nervous system where they mediate parenchymal inflammation, resulting in demyelination and clinical symptoms of an ascending paralysis. It is now generally recognised that the main cell type mediating EAE is the T helper type 17 (Th17) cell. Tolerance to EAE can be attained by DNA vaccination, but how the immune response against the myelin Ags is abrogated after DNA vaccination is not known. By employing short interfering RNA technology, induction of the innate immune signalling molecule interferon (IFN) -β was found to be necessary for the protective effect of DNA vaccination in EAE. In addition, DNA vaccination inhibited subsequent autoimmune Th17 cell responses. The Toll-like receptors (TLRs) of the innate immune system have evolved to recognise conserved molecular structures on microbes and signalling through them almost exclusively converge on the molecule MyD88. Signalling via MyD88 was found to be required for induction of EAE since mice deficient in this molecule did not develop disease. Upstream signalling via TLR4 and TLR9 had tolerogenic properties. In studies of Ag presentation in EAE, two major subtypes of dendritic cells (DCs) were examined. Plasmacytoid DCs were found to have a promoting role in the induction of EAE, partly via type 1 IFNs. Myeloid DCs had a redundant role in the induction phase of EAE, neither disease severity nor encephalitogenic Th17 responses were affected by their absence during priming. These studies further demonstrate that the cells and molecules of the innate immune system exhibit a crucial role in controlling the adaptive immune system which mediates tissue damage in autoimmune diseases.

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Ruppova, Klara. « Role of eosinophils in experimental autoimmune encephalomyelitis ». Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-231835.

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Experimental autoimmune encephalomyelitis (EAE) is the rodent model of multiple sclerosis (MS), a chronic autoimmune neuroinflammatory disease that has a devastating impact on various neurological functions of the patients. The hallmarks of both, MS and EAE, are neuroinflammation, demyelination and neuroaxonal degeneration. Various types of lymphoid and myeloid cells were shown to infiltrate the central nervous system and to participate in disease pathology. However, the role of eosinophil granulocytes has been less explored thus far. An early study showed that eosinophils infiltrate into the spinal cord of EAE mice and suggested their role in the disease progression. Recently, it was reported that eosinophils can play a protective role against EAE when mice are treated with an extract from helminths. Furthermore, it was shown that EAE development is not altered in mice deficient for interleukin-5, an important eosinophil pro-survival factor. Taken together, the role of eosinophils in EAE is currently unclear and needs to be investigated in detail. In the present study, we use the active model of EAE, whereby we immunized the C57BL/6 mouse strain with MOG35-55 peptide emulsified in the complete Freund’s adjuvant, in order to study a possible contribution of eosinophils to the disease pathology. Using the flow cytometry and RT-qPCR analysis of the spinal cord, we show that eosinophils infiltrate into the tissue in the course of EAE. The infiltration is likely driven by eosinophil chemoattractants, such as eotaxin-1, as the concentration of the latter was increased in the spinal cord during EAE, as shown on mRNA and protein level. Moreover, detailed flow cytometry analysis of spinal cord eosinophils revealed that they show signs of activation, namely an increase in CD11b and decrease in CCR-3 surface expression. Furthermore, we observed signs of degranulation of spinal cord eosinophils in EAE which was measured as a decrease of the side scatter parameter and an upregulation of CD63 surface expression. These data suggest a potential role of eosinophils in the pathology of EAE. In order to elucidate whether eosinophils are important for the disease development, eosinophil-deficient mice were subjected to EAE and the clinical development of the disease was observed. For this purpose, we used two independent models of eosinophil deficiency - ΔdblGATA1 and interleukin-5-depleted mice. ΔdblGATA1 mice are a genetically manipulated mouse strain bearing a deletion in GATA1 promoter that causes a specific depletion of eosinophils. Interestingly, clinical development of EAE was not affected in these mice when compared to their wild-type controls. As a next step, we depleted eosinophils by injecting wild-type mice with an antibody against the eosinophil pro-survival factor interleukin-5 in order to reduce eosinophil numbers in the effector phase of EAE. In accordance with the result from the experiment with ΔdblGATA1 mice, EAE progression was not altered in the eosinophil-depleted mice when compared to mice that were injected with an isotype control antibody. Further, we analyzed the neuroinflammation and demyelination in the spinal cord of 4ΔdblGATA1 mice subjected to EAE. Specifically, the infiltration of inflammatory cell populations, including CD4 and CD8 T cells, neutrophils and macrophages, was assessed by flow cytometry. In agreement with the unchanged clinical EAE development, inflammatory cell infiltration was not affected in ΔdblGATA1 mice. Furthermore, we analyzed expression of pro-inflammatory cytokines in the spinal cord of ΔdblGATA1 mice subjected to EAE in order to better characterize the inflammatory status. No significant changes were detected further confirming that eosinophils do not contribute to neuroinflammation in EAE. Finally, we assessed the demyelination in the spinal cord of ΔdblGATA1 EAE mice using luxol fast blue staining to detect myelin. In accordance with the unaffected clinical development and inflammatory status, we did not observe any difference in the spinal cord demyelination in ΔdblGATA1 mice when compared to their wild-type littermates. Taken together, although eosinophils infiltrate into the spinal cord of EAE mice and are activated and degranulate therein, they are dispensable for EAE development.

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Weissert, Robert. « Immunogenetics and treatment of experimental autoimmune encephalomyelitis / ». Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3645-5/.

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Lobell, Anna. « Suppressive DNA vaccination in experimental autoimmune encephalomyelitis / ». Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3782-6/.

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Dowdell, Kennichi C. « Neuroendocrine regulation of relapsing Experimental Autoimmune Encephalomyelitis / ». The Ohio State University, 1999. http://rave.ohiolink.edu/etdc/view?acc_num=osu1488191124569455.

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Wefer, Judit. « Studies of cellular pathogenesis in experimental autoimmune encephalomyelitis / ». Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-023-0/.

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Wållberg, Maja. « Modulation of immune responses in experimental autoimmune encephalomyelitis / ». Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-335-3/.

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Berl, Sabina [Verfasser]. « Neuronal Response to Experimental Autoimmune Encephalomyelitis / Sabina Berl ». Mainz : Universitätsbibliothek Mainz, 2020. http://d-nb.info/1203322933/34.

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Livres sur le sujet "Experimental Autoimmune Encephalomyelitis, Progesterone"

Weissert, Robert, dir. Experimental Autoimmune Encephalomyelitis - Models, Disease Biology and Experimental Therapy. InTech, 2012. http://dx.doi.org/10.5772/1190.

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Chiba, Kenji. Therapeutic Effects of the Sphingosine 1-Phosphate Receptor Modulator, Fingolimod (FTY720), on Experimental Autoimmune Encephalomyelitis. INTECH Open Access Publisher, 2012.

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Chapitres de livres sur le sujet "Experimental Autoimmune Encephalomyelitis, Progesterone"

Rao, Praveen, et Benjamin M. Segal. « Experimental Autoimmune Encephalomyelitis ». Dans Methods in Molecular Biology, 363–80. Totowa, NJ : Humana Press, 2012. http://dx.doi.org/10.1007/978-1-60761-720-4_18.

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Gran, B., K. O'Brien, D. Fitzgerald et A. Rostami. « Experimental Autoimmune Encephalomyelitis ». Dans Handbook of Neurochemistry and Molecular Neurobiology, 355–77. Boston, MA : Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-30398-7_16.

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Ballerini, Clara. « Experimental Autoimmune Encephalomyelitis ». Dans Methods in Molecular Biology, 375–84. New York, NY : Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1311-5_27.

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Jagessar, S. Anwar, Karin Dijkman, Jordon Dunham, Bert A. ‘t Hart et Yolanda S. Kap. « Experimental Autoimmune Encephalomyelitis in Marmosets ». Dans Methods in Molecular Biology, 171–86. New York, NY : Springer New York, 2014. http://dx.doi.org/10.1007/7651_2014_113.

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Terry, Rachael L., Igal Ifergan et Stephen D. Miller. « Experimental Autoimmune Encephalomyelitis in Mice ». Dans Methods in Molecular Biology, 145–60. New York, NY : Springer New York, 2014. http://dx.doi.org/10.1007/7651_2014_88.

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Encinas, J. A., et V. K. Kuchroo. « Genetics of Experimental Autoimmune Encephalomyelitis ». Dans Genes and Genetics of Autoimmunity, 247–72. Basel : KARGER, 1999. http://dx.doi.org/10.1159/000060485.

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Constantinescu, Cris S. « Environmental Influences in Experimental Autoimmune Encephalomyelitis ». Dans Experimental Models of Multiple Sclerosis, 523–46. Boston, MA : Springer US, 2005. http://dx.doi.org/10.1007/0-387-25518-4_25.

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Kieseier, Bernd C., et Hans-Peter Hartung. « Matrix Metalloproteinases in Experimental Autoimmune Encephalomyelitis ». Dans Advances in Experimental Medicine and Biology, 303–6. Boston, MA : Springer US, 1997. http://dx.doi.org/10.1007/978-1-4757-9613-1_39.

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Chan, Andrew, et Ralf Gold. « Apoptotic Cell Death in Experimental Autoimmune Encephalomyelitis ». Dans Experimental Models of Multiple Sclerosis, 507–21. Boston, MA : Springer US, 2005. http://dx.doi.org/10.1007/0-387-25518-4_24.

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Zaller, D. M., et V. S. Sloan. « Transgenic Mouse Models of Experimental Autoimmune Encephalomyelitis ». Dans Current Topics in Microbiology and Immunology, 15–31. Berlin, Heidelberg : Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-85208-4_2.

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Actes de conférences sur le sujet "Experimental Autoimmune Encephalomyelitis, Progesterone"

dos Santos Farias, Alessandro, et Fernanda Garcia Fossa. « B-lymphocytes characterization in experimental autoimmune encephalomyelitis ». Dans XXIII Congresso de Iniciação Científica da Unicamp. Campinas - SP, Brazil : Galoá, 2015. http://dx.doi.org/10.19146/pibic-2015-38297.

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Borin Pereira, Alexandre, Tabata R. Costa, Fernanda Garcia Fossa, Jéssica Funari, Guilherme Morais, Alessandro dos Santos Farias et Carolina Francelin Rovarotto. « Alterations in thymocyte subpopulations during the course of experimental autoimmune encephalomyelitis ». Dans XXIII Congresso de Iniciação Científica da Unicamp. Campinas - SP, Brazil : Galoá, 2015. http://dx.doi.org/10.19146/pibic-2015-38275.

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Maria Barbosa Dos Santos, Leonilda, Vanessa Cristina De Barros Mariano, Stephani Oliveira Alves, Vitor Almeida Da Silva et Fabiana Ferreira Aquino. « The effect of vitamin D in the evolution of experimental autoimmune encephalomyelitis ». Dans XXIII Congresso de Iniciação Científica da Unicamp. Campinas - SP, Brazil : Galoá, 2015. http://dx.doi.org/10.19146/pibic-2015-37964.

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RODRIGUES COSTA, TABATA, Alessandro Farias, Carolina Francelin Rovarotto, Fernando Pradella, GLEIDY A. SILVA, Alexandre Borin Pereira, Jéssica Funari et AFSAR Syed. « Analysis of CD4+RUNX3+ T lymphocytes during clinical course of experimental autoimmune encephalomyelitis ». Dans XXIV Congresso de Iniciação Científica da UNICAMP - 2016. Campinas - SP, Brazil : Galoa, 2016. http://dx.doi.org/10.19146/pibic-2016-51128.

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Maria Barbosa Dos Santos, Leonilda, et Amanda De Barros Piffer. « The effect of vitamin D in the evolution of experimental autoimmune encephalomyelitis. Effect on B-lymphocytes function ». Dans XXIII Congresso de Iniciação Científica da Unicamp. Campinas - SP, Brazil : Galoá, 2015. http://dx.doi.org/10.19146/pibic-2015-38190.

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Li, Chung-Hsien, Ming-Hong Lin, Yen-Fu Chen, Shih-Han Chu, Pang-Hsien Tu, Cheng-Chieh Fang, Chia-Hung Yen et al. « Abstract 1295 : Role of glycine N-methyltransferase in the regulation of T cell responses in experimental autoimmune encephalomyelitis ». Dans Proceedings : AACR 106th Annual Meeting 2015 ; April 18-22, 2015 ; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1295.

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Dalenogare, Diéssica Padilha, Diulle Spat Peres, Maria Fernanda Pessano Fialho et Gabriela Trevisan dos Santos. « Periorbital nociception in a progressive multiple sclerosis mouse model is dependent on TRPA1 channel activation ». Dans XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.610.

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Background: Headache is one of the main painful symptoms described by multiple sclerosis patients. Previously, it was described that neuropathic pain-like behaviors were dependent on transient receptor potential ankyrin 1 (TRPA1) activation in a progressive multiple sclerosis model induced by experimental autoimmune encephalomyelitis (PMS- EAE) in mice. Objective: Here, we aimed to investigate if periorbital mechanical allodynia induced by PMS-EAE was also related to TRPA1 activation. Design and setting: Federal University of Santa Maria, Santa Maria, RS, Brazil. Methods: To induce a PMS-EAE we used female C57BL/6 wild-type and TRPA1- deficient (Trpa1-/-) mice. By the von Frey test, periorbital mechanical allodynia development was observed, and the nociception peak occurred 14 days after induction. At nociception peak day, the mice were treated with sumatriptan, TRPA1 antagonists (HC-030031, A-967079, metamizole, and propyphenazone. Results: The development of mechanical allodynia was showed as well as the antinociceptive effects for all treatments in induced mice. A significant reduction of TRPA1 expression was detected. Conclusion: Thus, these results suggest that headache-like symptoms induced by the PMS-EAE mouse model might occurring by TRPA1 activation.

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