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Resident Macrophages Cloak Tissue Microlesions to Prevent Neutrophil-Driven Inflammatory Damage

Stefan Uderhardt1, Andrew J Martins2, John S Tsang2

  • 1Lymphocyte Biology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892, USA.

Cell
|April 9, 2019
PubMed

Insights

Tissue-resident macrophages prevent inflammatory damage by cloaking cell death, stopping neutrophil swarms. This mechanism maintains tissue homeostasis during cellular injury.

Area of Science:

  • Immunology
  • Cell Biology
  • Tissue Homeostasis

Background:

  • Neutrophils accumulate at sites of cell damage, exacerbating tissue disruption.
  • The role of inflammatory damage from neutrophil accumulation in cell death has been unclear.

Purpose of the Study:

  • To investigate whether inflammatory damage from neutrophil accumulation is an unavoidable consequence of cell death.
  • To explore the mechanisms by which tissue-resident macrophages respond to cell death.

Main Methods:

  • Dynamic intravital imaging
  • Confocal multiplex microscopy

Main Results:

  • Tissue-resident macrophages detect individual cell deaths.
  • Macrophages extend membrane processes to sequester cellular damage.
  • This "cloaking" mechanism prevents neutrophil chemoattractant signaling and swarm formation.
  • Neutrophil-mediated inflammatory damage is prevented, maintaining tissue homeostasis.

Conclusions:

  • Tissue-resident macrophages play a critical role in preventing inflammatory damage following cell death.
  • The macrophage "cloaking" mechanism is essential for maintaining tissue homeostasis during cellular injury.
  • This process mitigates the detrimental effects of neutrophil accumulation in damaged tissues.
Keywords:
anti-inflammationcloakingcollateral damagedamage responseinflammation preventionintravital imagingneutrophil swarmingresident macrophagestissue homeostasistissue protection

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