Pertussis vaccine-induced experimental autoimmune encephalomyelitis in mice

Abstract

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.

Evaluating the function of the Aryl Hydrocarbon Receptor in CNS autoimmunity

“…In order to increase disease incidence, pertussis toxin is often administered at the time of the immunological challenge and two days later 99 . On the other hand, passive EAE is induced by adoptive transfer of encephalitogenic T cells, which can be in vitro manipulated before being inoculated to the recipients.…”