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- W4313305911 abstract "Abstract In this study, we sought to understand how the microbiota regulates inflammatory mechanisms underlying cardiac autoimmunity. We employ an autoimmunization model of heart disease in mice, termed experimental autoimmune myocarditis (EAM). This disease model depends on CD4+ T cells for pathogenesis, immediately implying a cytokine product of these cells as a critical mediator of disease pathogenesis, and an attractive target for therapeutic intervention. Our laboratory has previously reported that Th17 cells are critical for the disease process. In order to establish a role for the commensal microbiota in autoimmune heart disease, we treated animals with a comprehensive polyantibiotic cocktail to induce antibiotic dysbiosis. Treating BALB/cJ animals with antibiotic limited the development of myocarditis, and furthermore prevented their progression to later heart failure. Segmented filamentous bacteria (SFB) represent a clade of Clostridia that have been found to elicit intestinal Th17 differentiation upon colonization, and subsequently modulate susceptibility to Th17-associated autoimmune disease. We colonized BALB/cJ mice with SFB and observed that these animals progress to diminished cardiac function following the induction of EAM. Microbiota manipulations were associated with differences in canonical Th17-associated programs, pointing to these pathways as an important mechanism in coupling commensal sensing to the progression of heart disease." @default.
- W4313305911 created "2023-01-06" @default.
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- W4313305911 date "2015-05-01" @default.
- W4313305911 modified "2023-09-25" @default.
- W4313305911 title "Commensal microbiota regulate inflammatory cardiac remodeling (BA6P.126)" @default.
- W4313305911 doi "https://doi.org/10.4049/jimmunol.194.supp.114.7" @default.
- W4313305911 hasPublicationYear "2015" @default.
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