Vascular adhesion and transendothelial migration of eosinophil leukocytes

Abstract

Tissues respond to injury with inflammation in an effort to protect and repair the damaged site. During inflammation, leukocytes typically accumulate in response to certain chemicals produced within the tissue itself. The passage of leukocytes through the vascular lumen into tissues occurs in several phases, including rolling, activation, firm adhesion, transendothelial migration, and subendothelial migration. Although infiltration of eosinophil leukocytes is one of the most important aspects of allergic inflammatory reactions, eosinophils also participate in nonallergic inflammation. Eosinophil accumulation is regulated not only by endothelial adhesion molecules, but also by interactions between eosinophil adhesion molecules and extracellular matrix elements. This review summarizes the regulation of eosinophil leukocyte adhesion and migration. A better understanding of eosinophil recruitment responses may lead to the development of novel therapeutics for chronic allergic diseases.

The role of the complement anaphylatoxins in the recruitment of eosinophils

“…Thus the eosinophil is correctly viewed as a tissue cell, which is found in the blood as it transits from the bone marrow to mucosal sites. Review articles dealing with the biology of eosinophils have been published recently [7][8][9].…”

High Vascular Endothelial Growth Factor Levels in NZW Mice Do Not Correlate with Collagen Deposition in Allergic Asthma

“…Eosinophils store cationic and cytotoxic proteins in their secondary granules, among them the eosinophil peroxidase (EPO), a cationic heme-containing protein that corresponds to nearly 25% of the total protein mass in eosinophil secondary granules [10]. EPO was shown to be cytotoxic to the epithelial cells of the bronchi [11], and in consequence, the airway smooth muscle becomes more reactive to various stimuli. This bronchial hyperreactivity (BHR) is one of the characteristic features of asthma.…”

Modulation of β1-integrins on hemopoietic progenitor cells after allergen challenge in asthmatic subjects

“…However, VLA-4 is just one of several adhesion molecules required for recruitment of eosinophils into inflamed tissues, and neutrophils rely entirely on selectins and b2-integrins (Mac-1 and LFA-1) for this process because they do not typically express VLA-4. 38,39,43 Because these adhesion molecules are also expressed on progenitor cells, lung migration is likely to progress despite reduced VLA-4 expression. Selectins were not a focus of this study, and LFA-1 was not examined because it does not appear necessary for BM cell retention 14 ; thus we can only speculate as to their role in lung homing at this time.…”

“…Mac-1 might instead function to mediate progenitor cell transmigration from the PB into the lung, as is the case for mature hemopoietic cells, such as eosinophils. 38,39 b1-Integrins mediate binding of CD34 1 cells to BM components, with VLA-5 binding to fibronectin while VLA-4 binds to both fibronectin and VCAM-1. 21,32,40,41 We established similar binding patterns for CD34 1 CD45 1 cells using SDF-1, a potent progenitor cell chemokine, 9,32,42 to induce adherence of BM-derived CD34 1 CD45 1 cells to fibronectin and VCAM-1: adhesion to VCAM-1 was VLA-4 dependent because anti-VLA-4 antibodies completely attenuated SDF-1-stimulated adhesion.…”