Sequential release of TNFα and phospholipase A(2) in a rat model of LPS-induced pleurisy

The levels of extracellular phospholipase A(2) (sPLA(2)) and TNFα, and cell accumulation were measured in the pleural washings obtained at different times following the induction of Escherichia coli lipopolysaccharide (LPS, 100 μg/cavity) pleurisy in rats. TNFα peaked at 2 hours (3036 ± 160.3 units/...

Descripción completa

Detalles Bibliográficos
Autores principales: Cicala, C., Bucci, M., D′Acquisto, F., Parente, L., Cirino, G.
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 1997
Materias:
Research Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2365826/
https://www.ncbi.nlm.nih.gov/pubmed/18472822
http://dx.doi.org/10.1080/09629359791703
Descripción
Sumario:The levels of extracellular phospholipase A(2) (sPLA(2)) and TNFα, and cell accumulation were measured in the pleural washings obtained at different times following the induction of Escherichia coli lipopolysaccharide (LPS, 100 μg/cavity) pleurisy in rats. TNFα 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-TNFα 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 TNFα which may be involved in the downregulation of sPLA(2) in this model of inflammation.

Ejemplares similares