Evidence that arachidonic acid derived from neutrophils and prostaglandin E2 are associated with the induction of acute lung inflammation by lipopolysaccharide of Escherichia coli
Evidence that arachidonic acid derived from neutrophils and prostaglandin E2 are associated with the induction of acute lung inflammation by lipopolysaccharide of Escherichia coli
复制标题
DOI:
10.1007/s00011-004-1308-7
复制
发表时间:
2004-12-01
影响因子:
6.7
通讯作者:
Sannomiya, P
中科院分区:
文献类型:
--
作者:
Alba-Loureiro, TC;Martins, EF;Sannomiya, P
Objective: The involvement of arachidonic acid (AA) and PGE(2) 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 lung vascular endothelium were used, as described below.Treatment: Rats were given an intratracheal injection of LPS (750 mug).Methods: Total and differential cell counts in BAL fluid; enzyme-linked immunoassay (ELISA) analyses of TNF-alpha, IL-1beta, LTB4 and PGE(2) in BAL, and immunohistochemical detection of ICAM-I 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 x 10(6) to 31.5 x 10(6) cells), accompanied by increased levels of TNF-alpha and IL-1beta (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 PGE(2) in BAL was increased by 3.5 fold, without changes in the levels of LTB4.Conclusions: These findings suggest that AA and PGE(2) are associated with LPS challenge.