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Updated: Apr 8, 2026
Determining Immune System Suppression versus CNS Protection for Pharmacological Interventions in Autoimmune Demyelination
Published on: September 12, 2016
Respiratory infection with a bacterial pathogen attenuates CNS autoimmunity through IL-10 induction
Sarah C Edwards1, Sarah C Higgins1, Kingston H G Mills1
1Immune Regulation Research Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin 2, Ireland.
Abstract:
Infection with viral or bacterial pathogens has been linked with the development of multiple sclerosis (MS), while infection with helminth parasites has been associated protection against MS and other autoimmune diseases. Here we have used a murine model of MS, experimental autoimmune encephalomyelitis (EAE), to examine the effect of infection with the respiratory pathogen Bordetella pertussis infection on development of CNS inflammation. The data demonstrate that infection of mice with B. pertussis significantly attenuates the clinical course of EAE induced by active immunization or cell transfer. This was reflected in a significant reduction in VLA-4 and LFA-1 expression on T cells and infiltration of IL-17(+), IFN-γ(+) and IFN-γ(+)IL-17(+) CD4 T cells into the CNS. Infection with B. pertussis induced IL-10 production from dendritic cells in vitro and enhanced the frequency of IL-10-producing CD25(-)Foxp3(+/-) CD4(+) T cells in vivo. Furthermore, the suppressive effects of B. pertussis infection on EAE were lost in IL-10(-/-) mice. Our findings demonstrate that a bacterial infection of the respiratory tract can attenuate EAE by promoting production of the anti-inflammatory cytokine IL-10 that may suppress licensing of autoaggressive T cells in the lungs, thereby preventing their migration into the CNS.
Insights
Bordetella pertussis infection significantly reduces multiple sclerosis (MS) severity in a mouse model by increasing IL-10 production. This suggests a potential therapeutic strategy for autoimmune diseases like MS.
Area of Science:
- Immunology
- Neuroscience
- Microbiology
Background:
- Infections are linked to autoimmune diseases like multiple sclerosis (MS).
- Helminth parasite infections show protective effects against MS.
- The impact of bacterial respiratory infections on MS development is unclear.
Purpose of the Study:
- To investigate the effect of Bordetella pertussis infection on the murine model of MS, experimental autoimmune encephalomyelitis (EAE).
- To understand the immunological mechanisms underlying B. pertussis-mediated protection against EAE.
Main Methods:
- Induction of EAE in mice followed by B. pertussis infection.
- Analysis of T cell activation markers (VLA-4, LFA-1) and cytokine profiles (IL-17, IFN-γ) in CD4 T cells.
- Assessment of IL-10 production by dendritic cells and CD4 T cells.
- Evaluation of EAE course in IL-10 knockout mice.
Main Results:
- B. pertussis infection significantly attenuated the clinical course of EAE.
- Reduced expression of VLA-4 and LFA-1 on T cells and decreased infiltration of inflammatory CD4 T cells (IL-17+, IFN-γ+) into the CNS.
- Increased IL-10 production by dendritic cells and CD4 T cells.
- Loss of EAE suppression in IL-10 knockout mice, highlighting IL-10's critical role.
Conclusions:
- Bordetella pertussis infection confers protection against experimental autoimmune encephalomyelitis.
- The protective effect is mediated by the induction of the anti-inflammatory cytokine IL-10.
- This mechanism may involve suppression of autoaggressive T cell activation in the lungs, preventing CNS migration.
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