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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-13386

Meyer, S; Z'graggen, B R; Blumenthal, S; Borgeat, A; Ganter, M T; Reyes, L; Booy, C; Neff, T A; Spahn, D R; Beck-Schimmer, B (2007). Hypoxia attenuates effector-target cell interaction in the airway and pulmonary vascular compartment. Clinical and Experimental Immunology, 150(2):358-367.

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Abstract

Leucocyte infiltration is known to play an important role in hypoxia-induced tissue damage. However, little information is available about hypoxia and interaction of effector (neutrophils) with target cells (alveolar epithelial cells, AEC; rat pulmonary artery endothelial cells, RPAEC). The goal of this study was to elucidate hypoxia-induced changes of effector-target cell interaction. AEC and RPAEC were exposed to 5% oxygen for 2-6 h. Intercellular adhesion molecule-1 (ICAM-1) expression was determined and cell adherence as well as cytotoxicity assays were performed. Nitric oxide and heat shock protein 70 (HSP70) production was assessed in target cells. Under hypoxic conditions enhanced ICAM-1 production was found in both cell types. This resulted in an increase of adherent neutrophils to AEC and RPAEC. The death rate of hypoxia-exposed target cells decreased significantly in comparison to control cells. Nitric oxide (NO) concentration was enhanced, as was production of HSP70 in AEC. Blocking NO production in target cells resulted in increased cytotoxicity in AEC and RPAEC. This study shows for the first time that target cells are more resistant to effector cells under hypoxia, suggesting hypoxia-induced cell protection. An underlying mechanism for this phenomenon might be the protective effect of increased levels of NO in target cells.

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Center for Integrative Human Physiology
04 Faculty of Medicine > Institute of Physiology
07 Faculty of Science > Institute of Physiology
DDC:570 Life sciences; biology
610 Medicine & health
Language:English
Date:November 2007
Deposited On:20 Mar 2009 09:14
Last Modified:27 Nov 2013 18:34
Publisher:Wiley-Blackwell
ISSN:0009-9104
Publisher DOI:10.1111/j.1365-2249.2007.03495.x
Official URL:http://www3.interscience.wiley.com/journal/117996404/abstract
PubMed ID:17892511
Citations:Web of Science®. Times Cited: 2
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