Linked Life Data

13680092

Source:http://linkedlifedata.com/resource/pubmed/id/13680092

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2003-11-17
pubmed:abstractText
This study characterizes the molecular neurotoxicity of diesel exhaust (DE) on the tachykinin substance P (SP) signaling system in the lungs. A total of 96 female Fischer 344/NH rats (approximately 175 g, approximately 4 weeks old) were randomly assigned to eight groups in a 2 x4 factorial design: capsaicin versus non-capsaicin (vehicle) pretreatment, and filtered room air versus two exposure levels of DE with diesel engine room control. The rats were exposed nose-only to room air or low (35.3 micro g/m(3)) and high concentrations (669.3 micro g/m(3)) particulates directly from a Cummins N14 research engine at 75% throttle for 4 h/day, 5 days/week, for 3 weeks. The findings showed that exposure to DE dose-dependently induced bronchopulmonary neurogenic inflammation, both in capsaicin- and vehicle-pretreated rats, as measured by plasma extravasation, edema, and inflammatory cells. DE inhalation affected the SP signaling processes, including stored SP depletion and the gene/protein overexpression for neurokinin-1 receptor. DE also significantly reduced the activity of neutral endopeptidase, a main degradation enzyme for SP. Consequently, these changes may be regarded as critical factors that switched neurogenic pulmonary responses from their protective functions to a detrimental role that perpetuates lung inflammation. These changes may possibly be associated with the mass concentration of DE particles due to their physico-chemical characteristics. Moreover, capsaicin-pretreated rats had more sensitivity to these levels of DE exposure due to stimulation of bronchopulmonary C-fibers. However, the effects of capsaicin treatment were not consistent and apparent in this study. Taken together, our findings suggest that neurokininergic mechanisms may possibly be involved in DE-induced lung inflammation, but that bronchopulmonary C-fibers did not dominate DE-induced inflammatory abnormalities.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0340-5761
pubmed:author
pubmed:issnType
Print
pubmed:volume
77
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
638-50
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:13680092-Animals, pubmed-meshheading:13680092-Bronchitis, pubmed-meshheading:13680092-Capsaicin, pubmed-meshheading:13680092-Endopeptidases, pubmed-meshheading:13680092-Female, pubmed-meshheading:13680092-Immunoenzyme Techniques, pubmed-meshheading:13680092-Immunohistochemistry, pubmed-meshheading:13680092-Nerve Fibers, Unmyelinated, pubmed-meshheading:13680092-Neurogenic Inflammation, pubmed-meshheading:13680092-Neurons, Afferent, pubmed-meshheading:13680092-Particle Size, pubmed-meshheading:13680092-Pneumonia, pubmed-meshheading:13680092-Radiopharmaceuticals, pubmed-meshheading:13680092-Rats, pubmed-meshheading:13680092-Rats, Inbred F344, pubmed-meshheading:13680092-Receptors, Neurokinin-1, pubmed-meshheading:13680092-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:13680092-Signal Transduction, pubmed-meshheading:13680092-Substance P, pubmed-meshheading:13680092-Technetium Tc 99m Aggregated Albumin, pubmed-meshheading:13680092-Vehicle Emissions
pubmed:year
2003
pubmed:articleTitle
Tachykinin substance P signaling involved in diesel exhaust-induced bronchopulmonary neurogenic inflammation in rats.
pubmed:affiliation
Center for Toxicology & Southwest Environmental Health Sciences Center and Department of Pediatrics, The University of Arizona, Tucson, Arizona, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S.