Low-dose interleukin 2 therapy halts the progression of post-streptococcal autoimmune complications in a rat model of rheumatic heart disease

ABSTRACT Acute rheumatic fever (ARF) is an autoimmune disease triggered by antibodies and T cells targeting the group A Streptococcus (GAS, Strep A) bacterium, often leading to rheumatic heart disease (RHD) and Sydenham’s chorea. Long-term monthly penicillin injections are recognized as a cornerston...

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Main Authors: Rukshan Ahamed Mohamed Rafeek, Natkunam Ketheesan, Michael F. Good, Manisha Pandey, Ailin Lepletier
Format: Article
Language:English
Published: American Society for Microbiology 2025-04-01
Series:mBio
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Online Access:https://journals.asm.org/doi/10.1128/mbio.03823-24
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author Rukshan Ahamed Mohamed Rafeek
Natkunam Ketheesan
Michael F. Good
Manisha Pandey
Ailin Lepletier
author_facet Rukshan Ahamed Mohamed Rafeek
Natkunam Ketheesan
Michael F. Good
Manisha Pandey
Ailin Lepletier
author_sort Rukshan Ahamed Mohamed Rafeek
collection DOAJ
description ABSTRACT Acute rheumatic fever (ARF) is an autoimmune disease triggered by antibodies and T cells targeting the group A Streptococcus (GAS, Strep A) bacterium, often leading to rheumatic heart disease (RHD) and Sydenham’s chorea. Long-term monthly penicillin injections are recognized as a cornerstone of public health programs to prevent Strep A reinfection and progression of ARF. However, compliance is poor, and better tools are required to slow disease progression. Preclinical evidence suggests that this can be achieved. Using a rat model that replicates post-streptococcal autoimmune complications, we explored the potential of low-dose interleukin-2 (LD-IL-2) as an immunotherapeutic intervention for ARF/RHD. In this model, injections of recombinant M protein from Strep A type 5 (rM5) to Lewis rats induce cardiac tissue inflammation, conduction abnormalities, and cross-reactive antibodies against cardiac and brain proteins central to disease pathogenesis. In animals injected with rM5 and treated with LD-IL-2, no cardiac functional or histological changes was observed. LD-IL-2 therapy effectively reduced the production of cross-reactive antibodies raised against host proteins and significantly increased regulatory T cells in the mediastinal lymph nodes. These novel findings suggest that LD-IL-2 will be an effective immunotherapeutic agent for treating ARF and has the potential to replace the standard monthly penicillin injections.IMPORTANCEPost-streptococcal autoimmune syndromes, including acute rheumatic fever, rheumatic heart disease, and Sydenham’s chorea, represent a significant yet often under-recognized health and economic burden. This is especially true in low-income countries and among Indigenous populations in high-income nations, where the disease burden is most severe. These conditions arise from an autoimmune response to group A Streptococcus infections, leading to long-term health complications, disability, and premature death. Despite their widespread impact, no vaccine is currently available to prevent reinfections, and no specific therapy exists to treat the resulting autoimmune process. This study uses a rat model of rheumatic heart disease to evaluate the potential of low-dose interleukin 2 therapy in improving clinical outcomes and reducing the incidence of autoimmune diseases triggered by streptococcal infections.
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spelling doaj-art-af3bc8aa6f3c42c7b46e6481d271049f2025-08-20T03:08:36ZengAmerican Society for MicrobiologymBio2150-75112025-04-0116410.1128/mbio.03823-24Low-dose interleukin 2 therapy halts the progression of post-streptococcal autoimmune complications in a rat model of rheumatic heart diseaseRukshan Ahamed Mohamed Rafeek0Natkunam Ketheesan1Michael F. Good2Manisha Pandey3Ailin Lepletier4School of Science and Technology, University of New England, New South Wales, AustraliaSchool of Science and Technology, University of New England, New South Wales, AustraliaInstitute for Biomedicine and Glycomics, Griffith University, Gold Coast, Queensland, AustraliaSchool of Science and Technology, University of New England, New South Wales, AustraliaSchool of Science and Technology, University of New England, New South Wales, AustraliaABSTRACT Acute rheumatic fever (ARF) is an autoimmune disease triggered by antibodies and T cells targeting the group A Streptococcus (GAS, Strep A) bacterium, often leading to rheumatic heart disease (RHD) and Sydenham’s chorea. Long-term monthly penicillin injections are recognized as a cornerstone of public health programs to prevent Strep A reinfection and progression of ARF. However, compliance is poor, and better tools are required to slow disease progression. Preclinical evidence suggests that this can be achieved. Using a rat model that replicates post-streptococcal autoimmune complications, we explored the potential of low-dose interleukin-2 (LD-IL-2) as an immunotherapeutic intervention for ARF/RHD. In this model, injections of recombinant M protein from Strep A type 5 (rM5) to Lewis rats induce cardiac tissue inflammation, conduction abnormalities, and cross-reactive antibodies against cardiac and brain proteins central to disease pathogenesis. In animals injected with rM5 and treated with LD-IL-2, no cardiac functional or histological changes was observed. LD-IL-2 therapy effectively reduced the production of cross-reactive antibodies raised against host proteins and significantly increased regulatory T cells in the mediastinal lymph nodes. These novel findings suggest that LD-IL-2 will be an effective immunotherapeutic agent for treating ARF and has the potential to replace the standard monthly penicillin injections.IMPORTANCEPost-streptococcal autoimmune syndromes, including acute rheumatic fever, rheumatic heart disease, and Sydenham’s chorea, represent a significant yet often under-recognized health and economic burden. This is especially true in low-income countries and among Indigenous populations in high-income nations, where the disease burden is most severe. These conditions arise from an autoimmune response to group A Streptococcus infections, leading to long-term health complications, disability, and premature death. Despite their widespread impact, no vaccine is currently available to prevent reinfections, and no specific therapy exists to treat the resulting autoimmune process. This study uses a rat model of rheumatic heart disease to evaluate the potential of low-dose interleukin 2 therapy in improving clinical outcomes and reducing the incidence of autoimmune diseases triggered by streptococcal infections.https://journals.asm.org/doi/10.1128/mbio.03823-24acute rheumatic feverrheumatic heart diseasegroup A streptococcuslow-dose interleukin-2immunotherapyautoimmune diseases
spellingShingle Rukshan Ahamed Mohamed Rafeek
Natkunam Ketheesan
Michael F. Good
Manisha Pandey
Ailin Lepletier
Low-dose interleukin 2 therapy halts the progression of post-streptococcal autoimmune complications in a rat model of rheumatic heart disease
mBio
acute rheumatic fever
rheumatic heart disease
group A streptococcus
low-dose interleukin-2
immunotherapy
autoimmune diseases
title Low-dose interleukin 2 therapy halts the progression of post-streptococcal autoimmune complications in a rat model of rheumatic heart disease
title_full Low-dose interleukin 2 therapy halts the progression of post-streptococcal autoimmune complications in a rat model of rheumatic heart disease
title_fullStr Low-dose interleukin 2 therapy halts the progression of post-streptococcal autoimmune complications in a rat model of rheumatic heart disease
title_full_unstemmed Low-dose interleukin 2 therapy halts the progression of post-streptococcal autoimmune complications in a rat model of rheumatic heart disease
title_short Low-dose interleukin 2 therapy halts the progression of post-streptococcal autoimmune complications in a rat model of rheumatic heart disease
title_sort low dose interleukin 2 therapy halts the progression of post streptococcal autoimmune complications in a rat model of rheumatic heart disease
topic acute rheumatic fever
rheumatic heart disease
group A streptococcus
low-dose interleukin-2
immunotherapy
autoimmune diseases
url https://journals.asm.org/doi/10.1128/mbio.03823-24
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