6533b7ddfe1ef96bd1274a42
RESEARCH PRODUCT
Sequential release of TNFα and phospholipase A2 in a rat model of LPS-induced pleurisy
Carla CicalaF. D′acquistoGiuseppe CirinoMariarosaria BucciLuca Parentesubject
medicine.medical_specialtyLipopolysaccharideImmunologypleurisyInflammationchemistry.chemical_compoundPhospholipase A2Downregulation and upregulationInternal medicinemedicineExtracellularlcsh:Pathologyratchemistry.chemical_classificationbiologybusiness.industrylipopolysaccharideCell Biologymedicine.diseaseEndocrinologyEnzymechemistryPleurisyImmunologybiology.proteinTumor necrosis factor alphaphospholipase A2medicine.symptombusinessResearch Articlelcsh:RB1-214description
The levels of extracellular phospholipase A2(sPLA2) and TNFα, and cell accumulation were measured in the pleural washings obtained at different times following the induction ofEscherichia colilipopolysaccharide (LPS, 100 μg/cavity) pleurisy in rats. TNFα peaked at 2 hours (3036 ± 160.3 units/ml) and decreased thereafter. Conversely, levels of sPLA2peaked 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 sPLA2enzyme is involved in LPS-induced pleurisy. The enzyme seems not to be stimulated by TNFα which may be involved in the downregulation of sPLA2in this model of inflammation.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 1997-01-01 | Mediators of Inflammation |