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Inflammation01:38

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Innate immune memory after brain injury drives inflammatory cardiac dysfunction.

Alba Simats1, Sijia Zhang2, Denise Messerer3

  • 1Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, Munich, Germany; Cerebrovascular Research Laboratory, Institute of Biomedical Research of Barcelona (IIBB), Spanish National Research Council (CSIC), Barcelona, Spain.

Cell
|July 23, 2024
PubMed
Summary

Stroke survivors may develop heart problems due to lingering immune system changes. Targeting interleukin-1 beta (IL-1β) and monocyte movement offers a new way to prevent these secondary stroke complications.

Keywords:
brain ischemiacardiac fibrosiscenicrivirocinnate immune memoryinterleukin-1myeloid cellsstrokesystemic inflammationtrained immunity

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Area of Science:

  • Immunology
  • Neurology
  • Cardiology

Background:

  • Stroke's long-term impact includes chronic comorbidities.
  • Systemic immune responses post-stroke are not well understood.
  • Myeloid innate immune memory is a potential cause of remote organ dysfunction.

Purpose of the Study:

  • To investigate the role of systemic immunity in post-stroke comorbidities.
  • To identify immunological mechanisms driving remote organ dysfunction after stroke.
  • To explore targeted immunotherapies for secondary stroke prevention.

Main Methods:

  • Single-cell sequencing to analyze immune cell changes.
  • In vivo mouse models of stroke and cardiac dysfunction.
  • Analysis of cardiac tissue from mice and human stroke patients.
  • Interleukin-1 beta (IL-1β) neutralization and CCR2/5 inhibition.

Main Results:

  • Persistent pro-inflammatory changes in monocytes/macrophages observed up to 3 months post-stroke.
  • Cardiac fibrosis and dysfunction were identified in mice and human patients.
  • IL-1β drives epigenetic changes in innate immune memory, inducing cardiac dysfunction.
  • Blocking IL-1β or CCR2/5 prevented post-stroke cardiac dysfunction.

Conclusions:

  • Myeloid innate immune memory contributes to remote organ dysfunction after stroke.
  • IL-1β is a key mediator of stroke-induced cardiac complications.
  • Targeting IL-1β and monocyte trafficking offers a therapeutic strategy for secondary stroke prevention.