ArticleIn vivo (Athens, Greece)
Effect of Decay-accelerating Factor on LPS-induced Acute Lung Injury in the Rat.
Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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5 authors.
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Abstract
BACKGROUND/
aimComplement activation has been implicated as a contributor to lung injury. Membrane-bound complement regulatory proteins, including decay-accelerating factor (DAF), control complement activation, thus mitigating complement-mediated injury. Their effect on lung injury remains unexplored. Using a DAF knockout rat model, we assessed the effect of DAF on the extent of lipopolysaccharide (LPS)-mediated acute lung injury (ALI) in rats. MATERIALS AND
methodsWild-type (WT) and DAF-knock out (
resultsLPS administration to WT rats caused histopathological lesions indicative of ALI and significantly increased infiltrating inflammatory cells, as well as total number of cells and interleukin (IL)-6 levels, in bronchoalveolar lavage fluid samples. DAF absence resulted in increased C3b levels in
conclusionDAF deficiency increased baseline C3b and C5aR1 protein levels in lung tissue. LPS-induced inflammatory response and lung injury were augmented in
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