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Updated: Jul 5, 2026

Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation
Published on: July 6, 2019
Sequential release of TNFalpha and phospholipase A(2) in a rat model of LPS-induced pleurisy
C Cicala1, M Bucci, F D Acquisto
1Department of Experimental Pharmacology University of Naples ]Federico II' Via D. Montesano 49 Naples 80131 Italy.
Abstract:
The levels of extracellular phospholipase A(2) (sPLA(2)) and TNFalpha, and cell accumulation were measured in the pleural washings obtained at different times following the induction of Escherichia coli lipopolysaccharide (LPS, 100 mug/cavity) pleurisy in rats. TNFalpha peaked at 2 hours (3036 +/- 160.3 units/ml) and decreased thereafter. Conversely, levels of sPLA(2) peaked at 48 hours (1.97 +/- 0.64 ng/ml) and were increased further (14.02 +/- 4.16 ng/ml) by pretreatment with anti-TNFalpha antibody. Cell accumulation was not affected by antibody pretreatment. These data indicate that the sPLA(2) enzyme is involved in LPS-induced pleurisy. The enzyme seems not to be stimulated by TNFalpha which may be involved in the downregulation of sPLA(2) in this model of inflammation.
