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Clara cell 10-KDA protein inhibits endotoxin-induced airway contraction in isolated perfused rat lungs
Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Occupational and Environmental Medicine. Östergötlands Läns Landsting, Pain and Occupational Centre, Occupational and Environmental Medicine Centre.
Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Occupational and Environmental Medicine.
Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Occupational and Environmental Medicine.
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2003 (English)In: Experimental Lung Research, ISSN 0190-2148, E-ISSN 1521-0499, Vol. 29, no 7, 455-473 p.Article in journal (Refereed) Published
Abstract [en]

Clara cell 10-kDa protein (CC10) is a major component of bronchoalveolar lavage fluid and is suggested to be a natural regulator of airway inflammation, possibly through its effects on theproin-flammatory enzyme(s), phospholipase A2. We examined the effect of recombinant human (rh) CC10 on endotoxin-induced airway contraction and cytokine release in isolated perfused rat lungs. We found that rhCC10 added to the lung perfusate abolished the endotoxin-induced airway contraction, and that it inhibited both the release of interleukin-1▀ and interleukin-6 into the lung perfusate and the release of tumor necrosis factors, into the pulmonary lavage fluid. By contrast, the levels of interferon-? were unaffected by CC10 administration. Rutin, a phospholipase A2 inhibitor, and N?-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, also attenuated the contraction induced by endotoxin. These findings demonstrate that rhCC10 inhibits endotoxin-induced airway contraction and the release of proinflammatory cytokines (interleukin-1▀, interleukin-6, and tumor necrosis factor-a) in isolated perfused rat lungs. The results also indicate that phospholipase A2 and nitric oxide are involved in the airway contraction in this model, possibly through their influence on the production of eicosanoids.

Place, publisher, year, edition, pages
2003. Vol. 29, no 7, 455-473 p.
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Medical and Health Sciences
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URN: urn:nbn:se:liu:diva-26519DOI: 10.1080/01902140303778Local ID: 11077OAI: oai:DiVA.org:liu-26519DiVA: diva2:247068
Available from: 2009-10-08 Created: 2009-10-08 Last updated: 2017-12-13

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Nosratabadi, Ali RezaLjungman, AndersLindahl, MatsTagesson, Christer

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