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

Author

Listed:
  • 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)

  • Kevin Mills
  • Johannes Riegler

    (Centre for Advanced Biomedical Imaging (CABI), University College London (UCL)
    Centre for Mathematics and Physics in the Life Sciences and Experimental Biology (CoMPLEX), 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)

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.

Suggested Citation

  • 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 Riegle, 2013. "Thymosin β4-sulfoxide attenuates inflammatory cell infiltration and promotes cardiac wound healing," Nature Communications, Nature, vol. 4(1), pages 1-10, October.
    • Handle: RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms3081
    DOI: 10.1038/ncomms3081
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