Journal
CLINICAL IMMUNOLOGY
Volume 141, Issue 2, Pages 187-196Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.clim.2011.08.003
Keywords
Endothelium; Leukocyte; Recruitment; Inflammation; IGIV; Anti-inflammatory
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Funding
- Bayer Healthcare
- Canadian Institutes of Heath Research [MG 7684, MGC 57081]
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High-dose intravenous immunoglobulin (IVIG) has anti-inflammatory effects via incompletely understood mechanisms. By investigating whether IVIG might modulate neutrophil (PMN) recruitment, we observed that IVIG dose-dependently inhibited (by 30-50%) PMN transendothetial migration (TEM) across human umbilical vein endothelial cells (EC) stimulated with IL-1 alpha, TNF-alpha or IL-1 beta + TNF-alpha. Inhibition required the presence of IVIG with the responding PMNs, was attributable to the F(ab)(2) portion and was unrelated to putative contaminants in IVIG. IVIG did not inhibit IL-1 beta- or TNF-alpha-induced increase of PMN adhesion to EC, nor did it affect C5a- or IL-8-induced PMN TEM across unstimulated EC. Effects of IVIG and F(ab)(2) fragments were not associated with PMN activation, assessed by CD62L shedding, CD11b upregulation or PMN shape. Thus, IVIG selectively inhibits PMN TEM across inflammatory-cytokine-stimulated - but not unstimulated - EC, perhaps contributing to therapeutic benefit in chronic inflammation with minimal impact on chemotactic-factor-induced PMN recruitment during acute infection. (C) 2011 Elsevier Inc. All rights reserved.
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