Linked Life Data

16809217

Source:http://linkedlifedata.com/resource/pubmed/id/16809217

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2006-6-30
pubmed:abstractText
The authors have previously shown that mechanical ventilation can result in increased pulmonary inflammation and suppressed peripheral leukocyte function. In the present study the effect of surfactant therapy on pulmonary inflammation and peripheral immune function in ventilated surfactant-deficient rats was assessed. Surfactant deficiency was induced by repeated lung lavage, treated rats with surfactant or left them untreated, and ventilated the rats during 2 hours. Nonventilated rats served as healthy control group. Expression of macrophage inflammatory protein (MIP)-2 was measured in bronchoalveolar lavage (BAL), interleukin (IL)-1beta, and heat shock protein 70 (HSP70) were measured in total lung homogenates. Outside the lung phytohemagglutinin (PHA)-induced lymphocyte proliferation, interferon (IFN)-gamma and IL-10 production, and natural killer activity were measured in splenocytes. After 2 hours of mechanical ventilation, expression of MIP-2, IL-1beta, and HSP70 increased significantly in the lungs of surfactant-deficient rats. Outside the lung, mitogen-induced proliferation and production of IFN-gamma and IL-10 reduced significantly. Only natural killer cell activity remained unaffected. Surfactant treatment significantly improved lung function, but could not prevent increased pulmonary expression of MIP-2, IL-1beta, and HSP70 and decreased peripheral mitogen-induced lymphocyte proliferation and IFN-gamma and IL-10 production in vitro. In conclusion, 2 hours of mechanical ventilation resulted in increased lung inflammation and partial peripheral leukocyte suppression in surfactant-deficient rats. Surfactant therapy ameliorated lung function but could not prevent or restore peripheral immunosuppression. The authors postulate that peripheral immunosuppression may occur in ventilated surfactant deficient patients, which may enhance susceptibility for infections.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0190-2148
pubmed:author
pubmed:issnType
Print
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-14
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:16809217-Animals, pubmed-meshheading:16809217-Bronchoalveolar Lavage Fluid, pubmed-meshheading:16809217-Carbon Dioxide, pubmed-meshheading:16809217-Cell Division, pubmed-meshheading:16809217-Chemokine CXCL2, pubmed-meshheading:16809217-Chemokines, CXC, pubmed-meshheading:16809217-Immunosuppression, pubmed-meshheading:16809217-Interferon-gamma, pubmed-meshheading:16809217-Interleukin-10, pubmed-meshheading:16809217-Killer Cells, Natural, pubmed-meshheading:16809217-Lung, pubmed-meshheading:16809217-Lung Compliance, pubmed-meshheading:16809217-Oxygen, pubmed-meshheading:16809217-Pneumonia, pubmed-meshheading:16809217-Pulmonary Surfactants, pubmed-meshheading:16809217-Rats, pubmed-meshheading:16809217-Rats, Sprague-Dawley, pubmed-meshheading:16809217-Respiration, Artificial, pubmed-meshheading:16809217-Spleen
pubmed:articleTitle
Exogenous surfactant restores lung function but not peripheral immunosuppression in ventilated surfactant-deficient rats.
pubmed:affiliation
Pediatric Intensive Care Unit, and Laboratory for Psycho-Neuroimmunology, University Medical Center Utrecht, Utrecht, The Netherlands.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't