• Barbara Fazekas, Siobhán Hamon, Carolina De Marco Verissimo, Krystyna Cwiklinski, Jesús López Corrales, Siobhán Gaughan, Sinéad Ryan, Clifford C Taggart, Sinéad Weldon, Matthew D Griffin, John P Dalton, and Richard Lalor.
• Molecular Parasitology Laboratory, Centre of One Health (COH), Ryan Institute, University of Galway, Galway, Ireland.
• Shock. 2025 Jan 1; 63 (1): 132140132-140.

AbstractSepsis results from a dysregulated host immune response to infection and is responsible for ~11 million deaths each year. In the laboratory, many aspects of sepsis can be replicated using a cecal ligation and puncture model, which is considered the most clinically relevant rodent model of sepsis. In the present study, histological and biomarker multiplex analyses revealed that the cecal ligation and puncture model initiated a large-scale inflammatory response in mice by 24 h, with evidence of acute organ damage by 48-72 h. While many typical proinflammatory cytokine/chemokines were systemically elevated, a specific array including IL-10, eotaxin, MIP-1α, MIP-1β, MCP-1, and RANTES noticeably increased just prior to animals reaching the humane endpoint. Treatment of mice with 10 μg of a synthetic 68-amino acid peptide derived from an immunomodulatory molecule secreted by a parasitic worm of humans and livestock, F. hepatica , termed F. hepatica helminth defense molecule, potently suppressed the systemic inflammatory profile, protected mice against acute kidney injury, and improved survival between 48 and 72 h after procedure. These results suggest that the anti-inflammatory parasite-derived F. hepatica helminth defense molecule peptide has potential as a biotherapeutic treatment for sepsis.Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the Shock Society.

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