The Use of Multiplexing to Identify Cytokine and Chemokine Networks in the Immune-Inflammatory Response to Trauma

Antioxid Redox Signal. 2021 Dec;35(16):1393-1406. doi: 10.1089/ars.2021.0054. Epub 2021 May 19.

Abstract

Significance: The immunoinflammatory responses that follow trauma contribute to clinical trajectory and patient outcomes. While remarkable advances have been made in trauma services and injury management, clarity on how the immune system in humans responds to trauma is lagging. Recent Advances: Multiplexing platforms have transformed our ability to analyze comprehensive immune mediator responses in human trauma. In parallel, with the establishment of large data sets, computational methods have been adapted to yield new insights based on mediator patterns. These efforts have added an important data layer to the emerging multiomic characterization of the human response to injury. Critical Issues: Outcome after trauma is greatly affected by the host immunoinflammatory response. Excessive or sustained responses can contribute to organ damage. Hence, understanding the pathophysiology behind traumatic injury is of vital importance. Future Directions: This review summarizes our work in the study of circulating immune mediators in trauma patients. Our foundational studies into dynamic patterns of inflammatory mediators represent an important contribution to the concepts and computational challenges that these large data sets present. We hope to see further integration and understanding of multiomics strategies in the field of trauma that can aid in patient endotyping and in potentially identifiying certain therapeutic targets in the future. Antioxid. Redox Signal. 35, 1393-1406.

Keywords: chemokines; cytokines; multiomics; multiple organ dysfunction syndrome; multiplexing; trauma.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Cytokines / immunology*
  • Humans
  • Immunity / immunology
  • Inflammation / immunology*
  • Wounds and Injuries / immunology*

Substances

  • Cytokines