Linked Life Data

17291600

Source:http://linkedlifedata.com/resource/pubmed/id/17291600

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-3
pubmed:dateCreated
2007-4-2
pubmed:abstractText
Substance P (SP) and calcitonin gene-related peptide (CGRP) released from capsaicin-sensitive afferents induce neurogenic inflammation via NK(1), NK(2) and CGRP1 receptor activation. This study examines the role of capsaicin-sensitive fibres and sensory neuropeptides in endotoxin-induced airway inflammation and consequent bronchial hyperreactivity with functional, morphological and biochemical techniques in mice. Carbachol-induced bronchoconstriction was measured with whole body plethysmography 24 h after intranasal lipopolysaccharide administration. SP and CGRP were determined with radioimmunoassay, myeloperoxidase activity with spectrophotometry, interleukin-1beta with ELISA and histopathological changes with semiquantitative scoring from lung samples. Treatments with resiniferatoxin for selective destruction of capsaicin-sensitive afferents, NK(1) antagonist SR 140333, NK(2) antagonist SR 48968, their combination, or CGRP1 receptor antagonist CGRP(8-37) were performed. Lipopolysaccharide significantly increased lung SP and CGRP concentrations, which was prevented by resiniferatoxin pretreatment. Resiniferatoxin-desensitization markedly enhanced inflammation, but decreased bronchoconstriction. CGRP(8-37) or combination of SR 140333 and SR 48968 diminished neutrophil accumulation, MPO levels and IL-1beta production, airway hyperresponsiveness was inhibited only by SR 48968. This is the first evidence that capsaicin-sensitive afferents exert a protective role in endotoxin-induced airway inflammation, but contribute to increased bronchoconstriction. Activation of CGRP1 receptors or NK(1)+NK(2) receptors participate in granulocyte accumulation, but NK(2) receptors play predominant role in enhanced airway resistance.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0167-0115
pubmed:author
pubmed:issnType
Print
pubmed:day
7
pubmed:volume
141
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
44-54
pubmed:dateRevised
2007-8-13
pubmed:meshHeading
pubmed-meshheading:17291600-Animals, pubmed-meshheading:17291600-Bronchial Hyperreactivity, pubmed-meshheading:17291600-Calcitonin Gene-Related Peptide, pubmed-meshheading:17291600-Capsaicin, pubmed-meshheading:17291600-Endotoxins, pubmed-meshheading:17291600-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:17291600-Female, pubmed-meshheading:17291600-Histocytochemistry, pubmed-meshheading:17291600-Inflammation, pubmed-meshheading:17291600-Interleukin-1beta, pubmed-meshheading:17291600-Lung, pubmed-meshheading:17291600-Mice, pubmed-meshheading:17291600-Mice, Inbred C57BL, pubmed-meshheading:17291600-Neurons, Afferent, pubmed-meshheading:17291600-Neuropeptides, pubmed-meshheading:17291600-Peroxidase, pubmed-meshheading:17291600-Radioimmunoassay, pubmed-meshheading:17291600-Somatostatin, pubmed-meshheading:17291600-Spectrophotometry, pubmed-meshheading:17291600-Substance P
pubmed:year
2007
pubmed:articleTitle
Role of capsaicin-sensitive afferents and sensory neuropeptides in endotoxin-induced airway inflammation and consequent bronchial hyperreactivity in the mouse.
pubmed:affiliation
Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, University of Pécs, H-7624 Pécs, Szigeti u. 12., Hungary.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't