Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2000-2-7
pubmed:abstractText
Alveolar macrophages (AM) are the primary resident effector cells in the alveolus. Leukotrienes (LT) are secreted by AM in their role as defender of the lung. 5-Lipoxygenase (5-LO) catalyzes the synthesis of LT in association with 5-LO-activating protein, termed "FLAP." AM demonstrate increased 5-LO metabolism compared to peripheral blood monocytes (PBM). Activated lymphocytes release mediators which upregulate 5-LO metabolism in PBM. The lymphocyte population of the lung consists predominantly of CD4+ helper constitutively "activated" T cells. We hypothesized that mediators released by pulmonary CD4+ T cells may upregulate and maintain of 5-LO metabolism in PBM as they enter the alveolar space and differentiate into AM. 5-LO metabolism in AM from CD4-depleted mice demonstrated reduced LT synthesis (LTC4: 66.9 +/- 8%; LTB4 61.4 +/- 6.2% control). The decrease in 5-LO metabolism was associated with reduced FLAP (30.1 +/- 14.5% of control) and 5-LO expression (49 +/- 13.7% of control). This defect in AM 5-LO metabolism in CD4-depleted mice was further associated with reduced LTC4 levels in bronchoalveolar lavage (BAL) fluid. In summary, factors secreted constitutively by lung lymphocytes, in particular CD4 cells, contribute to the increased 5-LO metabolism in AM.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0190-2148
pubmed:author
pubmed:issnType
Print
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
617-29
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:articleTitle
Regulation of 5-lipoxygenase metabolism in mononuclear phagocytes by CD4 T lymphocytes.
pubmed:affiliation
Division of Pulmonary, University of Michigan Medical Center, Ann Arbor 48109-0642, USA. mcoffey@umich.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't