rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
1995-8-24
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pubmed:abstractText |
Acid aspiration lung injury may be mediated primarily by neutrophils recruited to the lung by acid-induced cytokines. We hypothesized that a major acid-induced cytokine was IL-8 and that a neutralizing anti-rabbit-IL-8 monoclonal antibody (ARIL8.2) would attenuate acid-induced lung injury in rabbits. Hydrochloric acid (pH = 1.5 in 1/3 normal saline) or 1/3 normal saline (4 ml/kg) was instilled into the lungs of ventilated, anesthetized rabbits. The rabbits were studied for 6 or 24 h. In acid-instilled rabbits without the anti-IL-8 monoclonal antibody, severe lung injury developed in the first 6 h; in the long-term experiments, all rabbits died with lung injury between 12 and 14 h. In acid-instilled rabbits given the anti-IL-8 monoclonal antibody (2 mg/kg, intravenously) either as pretreatment (5 min before the acid) or as treatment (1 h after the acid), acid-induced abnormalities in oxygenation and extravascular lung water were prevented and extravascular protein accumulation was reduced by 70%; in the long-term experiments, anti-IL-8 treatment similarly protected lung function throughout the 24-h period. The anti-IL-8 monoclonal antibody also significantly reduced air space neutrophil counts and IL-8 concentrations. This study establishes IL-8 as a critical cytokine for the development of acid-induced lung injury. Neutralization of IL-8 may provide the first useful therapy for this clinically important form of acute lung injury.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/7615779-1008348,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7615779-1309402,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7615779-1416175,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7615779-1476206,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/7615779-1510812,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7615779-1556187,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7615779-1718038,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7615779-1726709,
http://linkedlifedata.com/resource/pubmed/commentcorrection/7615779-1755372,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/7615779-1918068,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/7615779-1969919,
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0021-9738
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:volume |
96
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
107-16
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:7615779-Animals,
pubmed-meshheading:7615779-Capillary Permeability,
pubmed-meshheading:7615779-Hemodynamics,
pubmed-meshheading:7615779-Hydrogen-Ion Concentration,
pubmed-meshheading:7615779-Interleukin-8,
pubmed-meshheading:7615779-Male,
pubmed-meshheading:7615779-Neutrophils,
pubmed-meshheading:7615779-Pneumonia, Aspiration,
pubmed-meshheading:7615779-Rabbits,
pubmed-meshheading:7615779-Tumor Necrosis Factor-alpha
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pubmed:year |
1995
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pubmed:articleTitle |
Acid aspiration-induced lung injury in rabbits is mediated by interleukin-8-dependent mechanisms.
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pubmed:affiliation |
Cardiovascular Research Institute, University of California San Francisco 94143-0130, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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