期刊
JOURNAL OF INFECTIOUS DISEASES
卷 218, 期 2, 页码 324-335出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jix637
关键词
Streptococcus pyogenes; group G streptococcus; acute rheumatic fever; rheumatic heart disease; rat autoimmune valvulitis
资金
- Australian National Health and Medical Research Council Project [1026753]
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 beta-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.-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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