Source:http://linkedlifedata.com/resource/pubmed/id/20463292
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2011-3-2
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pubmed:abstractText |
High-pressure ventilation induces barotrauma and pulmonary inflammation, thus leading to ventilator-induced lung injury (VILI). IL-22 has both immunoregulatory and tissue-protective properties. Functional IL-22 receptor expression is restricted to nonleukocytic cells, such as alveolar epithelial cells. When applied via inhalation, IL-22 reaches the pulmonary system directly and in high concentrations, and may protect alveolar epithelial cells against cellular stress and biotrauma associated with VILI. In A549 lung epithelial cells, IL-22 was able to induce rapid signal transducer and activator of transcription (STAT)-3 phosphorylation/activation, and hereon mediated stable suppressor of cytokine signaling (SOCS) 3 expression detectable even 24 hours after onset of stimulation. In a rat model of VILI, the prophylactic inhalation of IL-22 before induction of VILI (peak airway pressure = 45 cm H(2)O) protected the lung against pulmonary disintegration and edema. IL-22 reduced VILI-associated biotrauma (i.e., pulmonary concentrations of macrophage inflammatory protein-2, IL-6, and matrix metalloproteinase 9) and mediated pulmonary STAT3/SOCS3 activation. In addition, despite a short observation period of 4 hours, inhaled IL-22 resulted in an improved survival of the rats. These data support the hypothesis that IL-22, likely via activation of STAT3 and downstream genes (e.g., SOCS3), is able to protect against cell stretch and pulmonary baro-/biotrauma by enhancing epithelial cell resistibility.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Aerosols,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukins,
http://linkedlifedata.com/resource/pubmed/chemical/STAT3 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/STAT3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Stat3 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/interleukin-22
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
1535-4989
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
44
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
369-76
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pubmed:meshHeading |
pubmed-meshheading:20463292-Aerosols,
pubmed-meshheading:20463292-Animals,
pubmed-meshheading:20463292-Cell Line, Tumor,
pubmed-meshheading:20463292-Disease Models, Animal,
pubmed-meshheading:20463292-Epithelial Cells,
pubmed-meshheading:20463292-Humans,
pubmed-meshheading:20463292-Inflammation,
pubmed-meshheading:20463292-Interleukins,
pubmed-meshheading:20463292-Lung,
pubmed-meshheading:20463292-Lung Neoplasms,
pubmed-meshheading:20463292-Male,
pubmed-meshheading:20463292-Phosphorylation,
pubmed-meshheading:20463292-Rats,
pubmed-meshheading:20463292-Rats, Sprague-Dawley,
pubmed-meshheading:20463292-STAT3 Transcription Factor,
pubmed-meshheading:20463292-Ventilator-Induced Lung Injury
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pubmed:year |
2011
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pubmed:articleTitle |
Protective properties of inhaled IL-22 in a model of ventilator-induced lung injury.
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pubmed:affiliation |
Clinic for Anesthesiology, University Hospital of Ludwig-Maximilians-University, Munich, Germany. sandra.hoegl@med.uni-muenchen.de
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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