Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1997-2-13
pubmed:abstractText
1. The adult respiratory distress syndrome (ARDS) is an acute lung inflammation developed after direct or indirect contact with pathogenic agents. In the present study, a mouse model was developed to mimic this condition using aerosolized bacterial lipopolysaccharide (LPS) and to investigate the mechanisms involved in the lung inflammatory response. 2. Inhalation of LPS led to a time and dose-dependent increase in tumour necrosis factor-alpha (TNF-alpha) production and neutrophil recruitment into the bronchoalveolar lavage fluid (BALF) of Balb/c mice. Under the same conditions, neutrophil infiltration was also found in the BALF of the LPS-sensitive mouse strain C3H/HeN, but was absent in the LPS-resistant strain C3H/HeJ. Intranasal administration of murine recombinant TNF-alpha also triggered neutrophil recruitment. 3. One hour after inhalation of LPS, half of the maximal level of TNF-alpha was measured in the BALF, but only a few neutrophils were detected at this time. The peak TNF-alpha concentration was reached at 3 h, when the neutrophil amount started to increase. At 24 h, maximal neutrophil number was found in the BALF and TNF-alpha was no longer present. 4. Pretreatment of mice under different experimental conditions demonstrated that: (a) cycloheximide almost completely blocks both neutrophil recruitment and TNF-alpha production; (b) anti TNF-alpha antibodies block neutrophil recruitment; (c) indomethacin or aspirin enhance by two fold neutrophil recruitment; (d) indomethacin significantly increases TNF-alpha production 1 h after inhalation of LPS; (e) dibutyryl cyclic AMP and prostaglandin E2 (PGE2) block both neutrophil recruitment and TNF-alpha production. 5. It is concluded that aerosolized LPS in mice triggers an acute lung inflammation which can be used as a potential model of inhalational ARDS and that, strategies leading to the elevation of cyclic AMP levels in vivo can be effective in modulating LPS-induced TNF-alpha synthesis and neutrophil recruitment.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/8732293-1378868, http://linkedlifedata.com/resource/pubmed/commentcorrection/8732293-2053596, http://linkedlifedata.com/resource/pubmed/commentcorrection/8732293-2386959, http://linkedlifedata.com/resource/pubmed/commentcorrection/8732293-2541929, http://linkedlifedata.com/resource/pubmed/commentcorrection/8732293-2547721, http://linkedlifedata.com/resource/pubmed/commentcorrection/8732293-3510131, http://linkedlifedata.com/resource/pubmed/commentcorrection/8732293-3764421, http://linkedlifedata.com/resource/pubmed/commentcorrection/8732293-3805724, http://linkedlifedata.com/resource/pubmed/commentcorrection/8732293-3895437, http://linkedlifedata.com/resource/pubmed/commentcorrection/8732293-694537, http://linkedlifedata.com/resource/pubmed/commentcorrection/8732293-7507098, http://linkedlifedata.com/resource/pubmed/commentcorrection/8732293-7513521, http://linkedlifedata.com/resource/pubmed/commentcorrection/8732293-7532369, http://linkedlifedata.com/resource/pubmed/commentcorrection/8732293-7646623, http://linkedlifedata.com/resource/pubmed/commentcorrection/8732293-7694504, http://linkedlifedata.com/resource/pubmed/commentcorrection/8732293-7827287, http://linkedlifedata.com/resource/pubmed/commentcorrection/8732293-8003342, http://linkedlifedata.com/resource/pubmed/commentcorrection/8732293-8025736, http://linkedlifedata.com/resource/pubmed/commentcorrection/8732293-8027674, http://linkedlifedata.com/resource/pubmed/commentcorrection/8732293-8166294, http://linkedlifedata.com/resource/pubmed/commentcorrection/8732293-8181668, http://linkedlifedata.com/resource/pubmed/commentcorrection/8732293-8330899, http://linkedlifedata.com/resource/pubmed/commentcorrection/8732293-8388171
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0007-1188
pubmed:author
pubmed:issnType
Print
pubmed:volume
117
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1792-6
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:8732293-Administration, Inhalation, pubmed-meshheading:8732293-Animals, pubmed-meshheading:8732293-Antifungal Agents, pubmed-meshheading:8732293-Aspirin, pubmed-meshheading:8732293-Bronchoalveolar Lavage Fluid, pubmed-meshheading:8732293-Cyclic AMP, pubmed-meshheading:8732293-Cycloheximide, pubmed-meshheading:8732293-Cyclooxygenase Inhibitors, pubmed-meshheading:8732293-Disease Models, Animal, pubmed-meshheading:8732293-Escherichia coli, pubmed-meshheading:8732293-Indomethacin, pubmed-meshheading:8732293-Lipopolysaccharides, pubmed-meshheading:8732293-Lung, pubmed-meshheading:8732293-Male, pubmed-meshheading:8732293-Mice, pubmed-meshheading:8732293-Mice, Inbred BALB C, pubmed-meshheading:8732293-Mice, Inbred C3H, pubmed-meshheading:8732293-Neutrophils, pubmed-meshheading:8732293-Tumor Necrosis Factor-alpha
pubmed:year
1996
pubmed:articleTitle
Effect of cyclo-oxygenase inhibitors and modulators of cyclic AMP formation on lipopolysaccharide-induced neutrophil infiltration in mouse lung.
pubmed:affiliation
Unité de Pharmacologie Cellulaire, Unité Associée Institut Pasteur/INSERM 285, U.K.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't