Linked Life Data

18980502

Source:http://linkedlifedata.com/resource/pubmed/id/18980502

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2008-11-26
pubmed:abstractText
Although respiratory syncytial virus (RSV) infection is the most important cause of bronchiolitis in infants, the pathogenesis of RSV disease is poorly described. We studied histopathologic changes in a panel of lung tissue specimens obtained from infants with fatal cases of primary RSV infection. In these tissues, airway occlusion with accumulations of infected, apoptotic cellular debris and serum protein was consistently observed. Similar observations were found after RSV infection in New Zealand black (NZB) mice, which have constitutive deficiencies in macrophage function, but not in BALB/c mice. A deficiency in the number of alveolar macrophages in NZB mice appears to be central to enhanced disease, because depletion of alveolar macrophages in BALB/c mice before RSV exposure resulted in airway occlusion. In mice with insufficient numbers of macrophages, RSV infection yielded an increased viral load and enhanced expression of type I interferon-associated genes at the height of disease. Together, our data suggest that innate, rather than adaptive, immune responses are critical determinants of the severity of RSV bronchiolitis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0022-1899
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
198
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1783-93
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Macrophage impairment underlies airway occlusion in primary respiratory syncytial virus bronchiolitis.
pubmed:affiliation
Respiratory, Inflammation, and Autoimmunity Group, MedImmune, Gaithersburg, Maryland, USA. jennifer.reed@fda.hhs.gov
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't