Group G Streptococcus Induces an Autoimmune Carditis Mediated by Interleukin 17A and Interferon γ in the Lewis Rat Model of Rheumatic Heart Disease

Suchandan Sikder; Natasha L Williams; Alanna E Sorenson; Md A Alim; Miranda E Vidgen; Nicole J Moreland; Catherine M Rush; Robert S Simpson; Brenda L Govan; Robert E Norton; Madeleine W Cunningham; David J McMillan; Kadaba S Sriprakash; N Ketheesan

doi:10.1093/infdis/jix637

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Group G Streptococcus Induces an Autoimmune Carditis Mediated by Interleukin 17A and Interferon γ in the Lewis Rat Model of Rheumatic Heart Disease

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Group G Streptococcus Induces an Autoimmune Carditis Mediated by Interleukin 17A and Interferon γ in the Lewis Rat Model of Rheumatic Heart Disease

Suchandan Sikder, Natasha L Williams, Alanna E Sorenson, Md A Alim, Miranda E Vidgen, Nicole J Moreland, Catherine M Rush, Robert S Simpson, Brenda L Govan, Robert E Norton, …

Journal of Infectious Diseases, Vol.218(2), pp.324-335

2018

DOI: https://doi.org/10.1093/infdis/jix637

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Abstract

streptococcus pyogenes

group G streptococcus

acute rheumatic fever

rheumatic heart disease

rat autoimmune valvulitis

Acute rheumatic fever and rheumatic heart disease (ARF/RHD) have long been described as autoimmune sequelae of Streptococcus pyogenes or group A streptococcal (GAS) infection. Both antibody and T-cell responses against immunodominant GAS virulence factors, including M protein, cross-react with host tissue proteins, triggering an inflammatory response leading to permanent heart damage. However, in some ARF/RHD-endemic regions, throat carriage of GAS is low. Because Streptococcus dysgalactiae subspecies equisimilis organisms, also known as β-hemolytic group C streptococci and group G streptococci (GGS), also express M protein, we postulated that streptococci other than GAS may have the potential to initiate or exacerbate ARF/RHD. Using a model initially developed to investigate the uniquely human disease of ARF/RHD, we have discovered that GGS causes interleukin 17A/interferon γ-induced myocarditis and valvulitis, hallmarks of ARF/RHD. Remarkably the histological, immunological, and functional changes in the hearts of rats exposed to GGS are identical to those exposed to GAS. Furthermore, antibody cross-reactivity to cardiac myosin was comparable in both GGS- and GAS-exposed animals, providing additional evidence that GGS can induce and/or exacerbate ARF/RHD.

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Title: Group G Streptococcus Induces an Autoimmune Carditis Mediated by Interleukin 17A and Interferon γ in the Lewis Rat Model of Rheumatic Heart Disease
Authors: Suchandan Sikder (Author) - James Cook University
Natasha L Williams (Author) - James Cook University
Alanna E Sorenson (Author) - James Cook University
Md A Alim (Author) - James Cook University
Miranda E Vidgen (Author) - University of the Sunshine Coast, Queensland, School of Health and Sport Sciences - Legacy
Nicole J Moreland (Author) - University of Auckland, New Zealand
Catherine M Rush (Corresponding Author) - James Cook University
Robert S Simpson (Author) - Townsville Hospital
Brenda L Govan (Author) - James Cook University
Robert E Norton (Author) - Townsville Hospital
Madeleine W Cunningham (Author) - University of Oklahoma Health Sciences Center, United States
David J McMillan (Author) - University of the Sunshine Coast, Queensland, School of Health and Sport Sciences - Legacy
Kadaba S Sriprakash (Author) - QIMR Berghofer Medical Research Institute
N Ketheesan (Author) - James Cook University
Publication details: Journal of Infectious Diseases, Vol.218(2), pp.324-335
Publisher: Oxford University Press
Date published: 2018
DOI: 10.1093/infdis/jix637
ISSN: 0022-1899
Organisation Unit: University of the Sunshine Coast, Queensland; School of Health and Sport Sciences - Legacy; School of Science, Technology and Engineering; Centre for Bioinnovation
Language: English
Record Identifier: 99450862302621
Output Type: Journal article

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Web Of Science research areas: Immunology; Infectious Diseases; Microbiology

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