rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
8
|
pubmed:dateCreated |
1997-2-13
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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.
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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
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Apr
|
pubmed:issn |
0007-1188
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pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
117
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1792-6
|
pubmed:dateRevised |
2009-11-19
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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
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pubmed:year |
1996
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pubmed:articleTitle |
Effect of cyclo-oxygenase inhibitors and modulators of cyclic AMP formation on lipopolysaccharide-induced neutrophil infiltration in mouse lung.
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pubmed:affiliation |
Unité de Pharmacologie Cellulaire, Unité Associée Institut Pasteur/INSERM 285, U.K.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|