Eosinophil trafficking to sites of allergic inflammation

Immunol Rev. 2001 Feb;179:163-72. doi: 10.1034/j.1600-065x.2001.790116.x.

Abstract

Eosinophils play a prominent pro-inflammatory role in allergic inflammation. Studies utilizing flow chambers, intravital video-microscopy, and cytokine and adhesion molecule-deficient mice have provided important insight into the mechanisms of eosinophil trafficking in inflamed blood vessels and into tissues in vivo. While the bone marrow generation of eosinophils is finely regulated by interleukin (IL)-5, the trafficking of eosinophils into tissues is regulated by several cytokines, chemokines, and adhesion molecules with overlapping functions. Prospects for therapeutically inhibiting eosinophilic inflammation by inhibiting eosinophil adhesion to endothelium are dependent on an improved understanding of the relative importance of individual cytokines and adhesion molecules in regulating eosinophil adhesion to endothelium. Alternative strategies to inhibit eosinophilic inflammation include the use of immunostimulatory DNA sequences containing a CpG motif to act as a Th1 adjuvant to prevent Th2 responses associated with IL-5 and eosinophilia. Immunostimulatory DNA sequences do not induce eosinophil apoptosis, but function at the level of the bone marrow to inhibit the IL-5-induced bone marrow generation and release of eosinophils.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Adjuvants, Immunologic / pharmacology
  • Animals
  • Bone Marrow / drug effects
  • Cell Adhesion
  • Cell Adhesion Molecules / physiology
  • Chemokine CCL11
  • Chemokines / physiology
  • Chemokines, CC*
  • Chemotaxis, Leukocyte*
  • Cytokines / physiology
  • Endothelium, Vascular / cytology
  • Eosinophilia / immunology
  • Eosinophilia / pathology
  • Eosinophilia / prevention & control
  • Eosinophils / physiology*
  • Fibronectins / metabolism
  • Hematopoiesis / drug effects
  • Humans
  • Hypersensitivity / immunology
  • Hypersensitivity / pathology
  • Inflammation / immunology
  • Inflammation / pathology
  • Integrins / physiology
  • Interleukin-1 / physiology
  • Interleukin-5 / deficiency
  • Interleukin-5 / genetics
  • Interleukin-5 / physiology
  • Mice
  • Mice, Knockout
  • Th1 Cells / immunology
  • Th2 Cells / immunology
  • Tumor Necrosis Factor-alpha / physiology
  • Vaccines, DNA / pharmacology

Substances

  • Adjuvants, Immunologic
  • CCL11 protein, human
  • Ccl11 protein, mouse
  • Cell Adhesion Molecules
  • Chemokine CCL11
  • Chemokines
  • Chemokines, CC
  • Cytokines
  • Fibronectins
  • Integrins
  • Interleukin-1
  • Interleukin-5
  • Tumor Necrosis Factor-alpha
  • Vaccines, DNA