Experimental autoimmune encephalomyelitis (EAE) is characterized by appearance of anti-myelin autoantibodies in the blood and with the increased expression of MHC (major histocompatibility complex) class I and II antigens in the brain tissue. Although there is an evidence of possible linkage between influenza vaccination and development of autoimmune processes, the precise mechanisms of action of this vaccine on EAE-induction is still unclear. In this study, effects of influenza vaccine on clinical sign, antimyelin antibody titer in the blood by ELISA test and expression of MHC class I and II molecules immunohistochemistry were examined in the brain of C57BL mice with EAE. EAE was induced by MOG 35-55 protein in 16 of 32 mice. Influenza split vaccine was administered to eight MOG-induced EAE mice and to eight previously nontreated mice. A significant increase of anti-influenza antibody was detected in vaccinated mice compared to nontreated mice. Also, significant increase of antimyelin antibodies was detected in mice with EAE compared to vaccinated group without EAE and control group, respectively. In EAE-influenza vaccinated mice, a mild but not significant increase of antimyelin antibodies was detected, compared to EAE mice. High expression of MHC-II and mild expression of MHC-I were detected in the brain of mice with EAE. No expressions were detected in vaccinated and normal intact brains. Similar staining was found between EAE-vaccinated and EAE group in both MHC-I and MHC-II expression. The results obtained show that influenza vaccine has no significant influence on EAE induction and severity of autoimmune processes.
Myelin oligodendrocyte glycoprotein (MOG) is a protein widely used in the induction of experimental autoimmune encephalomyelitis (EAE) for studying human multiple sclerosis (MS). In C57BL/6 female mice aged eight weeks, we administered subcutaneously MOG35-55 peptide in CFA (complete Freund?s adjuvant) along with pertussis vaccine injected intraperitoneally. We observed the sign of flaccid tail as early as thirteen days post-immunization in five of twelve animals. Hematoxylin and eosin staining of paraffin-embedded sections of lymph nodes and spleen revealed the presence of germinal centers in the immunized animals. In the control group of animals, lymphoid follicles without germinal centers were observed. Immunohistochemical staining of spleen sections revealed an expression of MHC II molecules in the EAE-induced group. We would like to point out that even though the clinical signs are mild, the morphological changes are apparent in the lymph nodes and spleen of MOG35-55-immunized mice.
Background: A small dose of the Bordetella pertussis vaccine is used as an adjuvant for the induction of experimental autoimmune encephalomyelitis (EAE) in mice. The effects of two doses of the Pertussis vaccine on clinical signs, antibody titers, and the expression of CD4 and MHC molecules in brain tissue sections of mice with EAE were examined. Methodology: EAE was induced by spinal cord homogenate in Complete Freund adjuvant (CFA) in 30 of 40 C57BL/6 mice divided in groups: EAE mice with a small adjuvant dose of the Pertussis vaccine (EAE-1), EAE mice with a human dose of the Pertussis vaccine (EAE-2), EAE mice (EAE-3). Results: None of the mice from the EAE groups progressed to severe EAE. Five mice from the EAE-2 group were found dead on the 13th day post-immunization. A significant increase of anti-MOG (myelin oligodendrocyte glycoprotein) antibodies was detected in mice with EAE compared to non-treated mice. Myelin loss and brain tissue lesions were observed in EAE-1 and EAE-2 mice compared to EAE-3 and non-treated mice. A high expression of MHC-II and a mild expression of MHC-I was detected in the brains of mice with EAE. No expressions were detected in intact brains. Scattered CD4-positive cells were detected in the brains of EAE-1 and EAE-2 mice compared to EAE-3 and non-treated mice. Conclusion: A small dose of the Bordetella pertussis vaccine could maintain the developed clinical signs and histological changes in mice with EAE, while higher doses led to additional adverse effects. The expression of CD4 and MHC class I and II molecules, as well as an increase in anti-MOG antibodies could be used as markers capable of monitoring the development and progression of EAE.
Literature data suggest possible link between influenza vaccination and development of autoimmune processes. Therefore, the aim of the study was to investigate the effect of influenza vaccination on spatial learning in mice with experimental autoimmune encephalomyelitis (EAE). EAE was induced in eight-week-old C57BL/6J female mice by subcutaneous immunization (MOG35–55 in complete Freund’s adjuvant) and Pertussis vaccine injected intraperitoneally. Mice were vaccinated with influenza vaccine three days before MOG immunization. The hippocampal-dependent spatial learning test, Morris Water Maze test (MWM), was performed before and after EAE induction. Significant difference (P < 0.05) in the time for completing the Morris Water Maze task was found between mice with mild clinical signs of EAE when compared to other mice. However no significant difference was observed between mice with EAE and mice with EAE that were vaccinated with influenza vaccine. Hippocampal tissue lesions in EAE mice are in correlation with memory impairment. Study shows no influence of influenza vaccine on progression of clinical signs of EAE, spatial learning and memory impairment.
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