| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Florida A & M University, College of Pharmacy and Pharmaceutical Sciences, Tallahassee, Florida 32307
Eosinophilic leukocytes have been implicated as primary effector cells in inflammatory and allergic diseases. When activated by cytokines, human eosinophils secrete and produce a variety of proinflammatory or tissue damaging substances. Although well known for their chemoattractant effects, little is known about the precise contribution of the eosinophil-selective chemokines, eotaxin, eotaxin-2, and eotaxin-3 to the effector functions of eosinophils. This forms the central focus of these investigations for which clone 15-HL-60 human eosinophilic cells were used as the in vitro model. Investigation results suggest that all three subtypes of eotaxin directly stimulate eosinophil superoxide anion generation that is inhibited by neutralizing eotaxin antibody or pretreatment of cells with the receptor antibody anti-CCR3. Pretreatment or co-treatment with each of the eotaxins augmented phorbol myristate-induced superoxide generation. Concentration-dependent degranulation of eosinophil peroxidase was noted for all three chemokines, and potentiation of calcium ionophore-induced degranulation was observed with eotaxin pretreatments. Results of interleukin-5 pretreatment studies suggest that the eotaxin chemokines may act cooperatively to enhance effector functions of eosinophils. Collectively, the present studies have advanced knowledge of the eotaxin family of chemokines to include eosinophil priming and modulation of eosinophil activation and secretion effector functions.
Key Words: eotaxin • eotaxin-2 • eotaxin-3 • human eosinophils • superoxide anion • eosinophil peroxidase
This article has been cited by other articles:
|
|
 |
|
  T. R. Johnson, M. E. Rothenberg, and B. S. Graham Pulmonary eosinophilia requires interleukin-5, eotaxin-1, and CD4+ T cells in mice immunized with respiratory syncytial virus G glycoprotein J. Leukoc. Biol., September 1, 2008; 84(3): 748 - 759. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Takashi, J. Park, S. Fang, S. Koyama, I. Parikh, and K. B. Adler A Peptide Against the N-Terminus of Myristoylated Alanine-Rich C Kinase Substrate Inhibits Degranulation of Human Leukocytes In Vitro Am. J. Respir. Cell Mol. Biol., June 1, 2006; 34(6): 647 - 652. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. O. Abonyo, M. S. Alexander, and A. S. Heiman Autoregulation of CCL26 synthesis and secretion in A549 cells: a possible mechanism by which alveolar epithelial cells modulate airway inflammation Am J Physiol Lung Cell Mol Physiol, September 1, 2005; 289(3): L478 - L488. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Correale and M. Fiol Activation of humoral immunity and eosinophils in neuromyelitis optica Neurology, December 28, 2004; 63(12): 2363 - 2370. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. Ogilvie, S. Paoletti, I. Clark-Lewis, and M. Uguccioni Eotaxin-3 is a natural antagonist for CCR2 and exerts a repulsive effect on human monocytes Blood, August 1, 2003; 102(3): 789 - 794. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
