Evidence that arachidonic acid derived from neutrophils and prostaglandin E2 are associated with the induction of acute lung inflammation by lipopolysaccharide of Escherichia coli
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Objective: The involvement of arachidonic acid (AA) and PGE2 during the E. coli lipopolysaccharide (LPS)-induced acute lung injury was investigated.
Material: Adult male Wistar rats were used. For in vitro studies, rat neutrophils, bronchoalveolar lavage (BAL) fluid, and lug vascular endothelium were used, as described below.
Treatment: Rats were given an intratracheal injection of LPS (750 μg).
Methods: Total and differential cell counts in BAL fluid; enzyme-linked immunoassay (ELISA) analyses of TNF-α, IL-1β, LTB4 and PGE2 in BAL, and immunohistochemical detection of ICAM-1 on lung vascular endothelium were performed six h after LPS challenge. Fatty acid composition of blood neutrophils and plasma was analyzed by HPLC.
Results: Rats instilled with LPS presented a sixty three-fold increase in the number of neutrophils in BAL (from 0.5 × 106 to 31.5 × 106 cells), accompanied by increased levels of TNF-α and IL-1β (p < 0.001), and a three-fold increase in ICAM-1 expression on vascular endothelium. The content of AA in blood neutrophils was reduced by 50%, whereas the level of PGE2 in BAL was increased by 3.5 fold, without changes in the levels of LTB4.
Conclusions: These findings suggest that AA and PGE2 are associated with LPS challenge.
Key words.Neutrophils Lipopolysaccharide Acute lung injury PGE2 Arachidonic acid
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