Linked Life Data

10194181

Source:http://linkedlifedata.com/resource/pubmed/id/10194181

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4 Pt 1
pubmed:dateCreated
1999-5-17
pubmed:abstractText
In order to assess inflammatory features related to severe asthma as compared with mild asthma, we investigated the secretion of 92 kDa gelatinase matrix metalloproteinase (MMP-9) in bronchial lavages of six patients undergoing mechanical ventilation (MV) for status asthmaticus (SA) and in six patients with mild asthma. Ten healthy nonventilated patients and four patients under MV without preexisting respiratory disease were also investigated. Patients with SA were characterized by prominent neutrophilic inflammation (82 +/- 4% versus 10% in mild asthma). On the basis of enzymatic and immunological analysis, results showed an acute 10- to 160-fold increase of 92 kDa gelatinase (MMP-9) concentration in epithelial lining fluid (ELF) from patients with SA, together with activated forms (46 and 26 kDa) of stromelysin-1 matrix metalloproteinase (MMP-3) and detectable concentration of free metallogelatinolytic activity (1-5 micrograms gelatin hydrolyzed/48 h/ml ELF). Concomitant elevated level of tissue inhibitor of metalloproteinase-1 (TIMP-1) was shown only in patients with SA, thus counterbalancing, at least partially, excess of activated 92 kDa gelatinase. Acutely enhanced albumin levels were only observed in patients with SA; in addition, 92 kDa gelatinase and albumin levels were significantly and positively correlated (r = 0.96, p < 0.0001), suggesting that 92 kDa gelatinase may account for increased bronchial permeability in patients with SA. Several arguments support that 92 kDa gelatinase during SA originates both from numerous activated chemoattracted neutrophils and from activated bronchial epithelial cells in response to in situ lung injury. The fact that no relevant change in ELF, albumin, MMP-9, MMP-3, TIMP-1, or laminin degradation products was observed during mild asthma, strongly supports that the mechanism of airway inflammation in SA is quite distinct from that observed in mild asthma.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1073-449X
pubmed:author
pubmed:issnType
Print
pubmed:volume
159
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1298-307
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10194181-Adult, pubmed-meshheading:10194181-Albumins, pubmed-meshheading:10194181-Asthma, pubmed-meshheading:10194181-Body Water, pubmed-meshheading:10194181-Bronchi, pubmed-meshheading:10194181-Bronchoalveolar Lavage Fluid, pubmed-meshheading:10194181-Bronchoscopy, pubmed-meshheading:10194181-Collagenases, pubmed-meshheading:10194181-Enzyme Activation, pubmed-meshheading:10194181-Epithelium, pubmed-meshheading:10194181-Humans, pubmed-meshheading:10194181-Inflammation, pubmed-meshheading:10194181-Laminin, pubmed-meshheading:10194181-Matrix Metalloproteinase 3, pubmed-meshheading:10194181-Matrix Metalloproteinase 9, pubmed-meshheading:10194181-Middle Aged, pubmed-meshheading:10194181-Peroxidase, pubmed-meshheading:10194181-Status Asthmaticus, pubmed-meshheading:10194181-Tissue Inhibitor of Metalloproteinase-1, pubmed-meshheading:10194181-Urea
pubmed:year
1999
pubmed:articleTitle
Contribution of 92 kDa gelatinase/type IV collagenase in bronchial inflammation during status asthmaticus.
pubmed:affiliation
INSERM U492 de Physiopathologie et Thérapeutique Respiratoires, Faculté de Médecine, Créteil, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't