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Resolvin E1 promotes mucosal surface clearance of neutrophils: a new paradigm for inflammatory resolution

Eric L Campbell1, Nancy A Louis, Sarah E Tomassetti

  • 1Mucosal Inflammation Program, Division of Gastroenterology, University of Colorado Health Science Center, Denver, CO 80262, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|May 15, 2007
PubMed

Insights

Resolvin E1 (RvE1) resolves inflammation by reducing neutrophil migration and promoting their clearance via CD55 on epithelial cells, offering a new model for inflammatory resolution.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Medicine

Background:

  • Neutrophil migration across epithelia is key in mucosal diseases.
  • Endogenous resolution mechanisms for these lesions are not fully understood.
  • Resolvins' effects on epithelial interactions and actions are less clear.

Purpose of the Study:

  • To investigate resolvin E1 (RvE1) effects on leukocyte transepithelial migration.
  • To explore RvE1's influence on neutrophil-epithelial interactions.
  • To elucidate the role of epithelial cells in RvE1-mediated resolution.

Main Methods:

  • Studied neutrophil transepithelial migration dynamics with RvE1 and chemerin.
  • Analyzed epithelial ChemR23 activation effects on neutrophil clearance.
  • Screened for PMN ligands on epithelial cells induced by RvE1.
  • Performed CD55 promoter analysis and used neutralizing antibodies.

Main Results:

  • RvE1 and chemerin reduced neutrophil transepithelial migration concentration-dependently.
  • Epithelial ChemR23 activation enhanced apical neutrophil clearance.
  • RvE1 selectively induced CD55, an antiadhesive molecule, on epithelial cells.
  • RvE1 and chemerin activated the CD55 promoter; CD55 inhibition blocked RvE1-mediated clearance.

Conclusions:

  • Proposed a 'two-hit' model for inflammatory resolution.
  • RvE1 receptor activation on neutrophils attenuates migration.
  • RvE1 actions on epithelia promote CD55-dependent neutrophil clearance.
  • This highlights active inflammatory resolution mechanisms at the epithelial surface.

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