Thymosin β4-sulfoxide attenuates inflammatory cell infiltration and promotes cardiac wound healing

Mark A. Evans, Nicola Smart, Karina N. Dubé, Sveva Bollini, James E. Clark, Hayley G. Evans, Leonie S. Taams, Rebecca Richardson, Mathieu Lévesque, Paul Martin, Kevin Mills, Johannes Riegler, Anthony N. Price, Mark F. Lythgoe and Paul R. Riley ()
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Mark A. Evans: Anatomy and Genetics, Sherrington Building, University of Oxford
Nicola Smart: Anatomy and Genetics, Sherrington Building, University of Oxford
Karina N. Dubé: Anatomy and Genetics, Sherrington Building, University of Oxford
Sveva Bollini: Anatomy and Genetics, Sherrington Building, University of Oxford
James E. Clark: Kings College London, Rayne Institute, St Thomas’ Hospital
Hayley G. Evans: Centre for Molecular and Cellular Biology of Inflammation (CMCBI), Infection and Inflammatory Disease, King’s College London
Leonie S. Taams: Centre for Molecular and Cellular Biology of Inflammation (CMCBI), Infection and Inflammatory Disease, King’s College London
Rebecca Richardson: Physiology and Pharmacology, School of Medical Sciences, University of Bristol, University Walk
Mathieu Lévesque: Physiology and Pharmacology, School of Medical Sciences, University of Bristol, University Walk
Paul Martin: Physiology and Pharmacology, School of Medical Sciences, University of Bristol, University Walk
Johannes Riegler: Centre for Advanced Biomedical Imaging (CABI), University College London (UCL)
Anthony N. Price: MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College London
Mark F. Lythgoe: Centre for Advanced Biomedical Imaging (CABI), University College London (UCL)
Paul R. Riley: Anatomy and Genetics, Sherrington Building, University of Oxford

Nature Communications, 2013, vol. 4, issue 1, 1-10

Abstract: Abstract The downstream consequences of inflammation in the adult mammalian heart are formation of a non-functional scar, pathological remodelling and heart failure. In zebrafish, hydrogen peroxide released from a wound is the initial instructive chemotactic cue for the infiltration of inflammatory cells, however, the identity of a subsequent resolution signal(s), to attenuate chronic inflammation, remains unknown. Here we reveal that thymosin β4-sulfoxide lies downstream of hydrogen peroxide in the wounded fish and triggers depletion of inflammatory macrophages at the injury site. This function is conserved in the mouse and observed after cardiac injury, where it promotes wound healing and reduced scarring. In human T-cell/CD14+ monocyte co-cultures, thymosin β4-sulfoxide inhibits interferon-γ, and increases monocyte dispersal and cell death, likely by stimulating superoxide production. Thus, thymosin β4-sulfoxide is a putative target for therapeutic modulation of the immune response, resolution of fibrosis and cardiac repair.

Date: 2013
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DOI: 10.1038/ncomms3081

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