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  • Title: Neutrophils from chronic granulomatous disease fail to increase endothelial permeability.
    Author: Kaslovsky RA, Gibbs L, Malik AB.
    Journal: Am J Physiol; 1991 Oct; 261(4 Pt 2):H1226-30. PubMed ID: 1656787.
    Abstract:
    Studies of neutrophil-dependent endothelial injury were made using normal neutrophils (nl-PMN, i.e., normal polymorphonuclear neutrophils) and PMN obtained from a patient with X-linked chronic granulomatous disease (CGD-PMN). Layering of nl-PMN on bovine pulmonary microvessel endothelial monolayers (ratio 10:1) followed by challenge with phorbol 12-myristate 13-acetate (PMA; 5 x 10(-9) M) resulted in a 190% increase in 125I-labeled albumin permeability across the monolayers. Pretreatment of endothelial monolayers with tumor necrosis factor-alpha (TNF-alpha; 200 or 1,000 U/ml) further enhanced the increase in permeability after stimulation of nl-PMN with PMA. In contrast, challenge of CGD-PMN layered on endothelial cells with PMA did not increase permeability, and the effect was not enhanced by pretreating the endothelial cells with TNF-alpha. Nl-PMN, but not CGD-PMN, generated superoxide anion on stimulation with PMA (42.5 +/- 0.7 vs. 6.5 +/- 0.6 nM.10(6) PMN-1.h-1). PMA also induced degranulation of nl-PMN as measured by release of elastase (2.32 +/- 0.12 micrograms/10(6) PMN) and myeloperoxidase (173.8 +/- 1.9 U/10(6) PMN) into the medium, whereas release by CGD-PMN was markedly reduced (elastase release of 0.88 +/- 0.04 microgram/10(6) PMN and myeloperoxidase release of 82.6 +/- 19.4 U/10(6) PMN). The adherence response of nl-PMN and CGD-PMN to the endothelial cells after PMA stimulation was similar (79.5 +/- 11.8% nl-PMN and 64.0 +/- 1.9% CGD-PMN). Therefore, the PMN respiratory burst, with the resultant generation of oxidants and PMN-derived proteases, is required to increase endothelial permeability even in the face of increased endothelial adhesivity.
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