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Phospholipase A2-induced pleural inflammation in rats
B M Weichman1, J W Berkenkopf, L A Marshall
1Division of Immunopharmacology, Wyeth-Ayerst Research, Princeton, NJ 08543.
Abstract:
Injection of Naja mocambique mocambique phospholipase A2 [PLA2] into the rat pleural cavity induced dose- and time-dependent fluid accumulation and cellular infiltration. The time course of the cell influx was initially neutrophilic [2-6 h] and later mononuclear [6-24 h]. During reverse passive Arthus reaction [RPAR] induced pleurisy, endogenously produced PLA2 activity, quantitated by the hydrolysis of [3H]-arachidonic acid E. coli substrate, was detected in the pleural exudate. However, the biosynthesis of eicosanoids and plasma extravasation in the pleural cavity preceded the 9-fold elevation in PLA2 activity which was obtained at 4 h. Whereas the exact role of PLA2 in the inflammatory response remains to be determined, these results demonstrate that exogenous PLA2 can induce pleural inflammation in the rat, and that this enzyme is released endogenously during experimental pleurisy.
Insights
Phospholipase A2 (PLA2) from Naja mocambique mocambique snake venom causes inflammation in rat pleural cavities. This enzyme is also released during experimental pleurisy, though its exact role in inflammation requires further study.
Area of Science:
- Biochemistry
- Toxicology
- Immunology
Background:
- Phospholipase A2 (PLA2) is an enzyme involved in inflammatory processes.
- The specific role of PLA2 in pleural inflammation is not fully understood.
Purpose of the Study:
- To investigate the effects of exogenous Naja mocambique mocambique phospholipase A2 (PLA2) on rat pleural inflammation.
- To determine if endogenous PLA2 is released during experimental pleurisy.
Main Methods:
- Rats were injected with varying doses of Naja mocambique mocambique PLA2 into the pleural cavity.
- Cellular infiltration and fluid accumulation were measured over time.
- PLA2 activity in pleural exudate was quantified during reverse passive Arthus reaction (RPAR) induced pleurisy.
Main Results:
- Exogenous PLA2 induced dose- and time-dependent pleural fluid accumulation and cellular infiltration.
- Neutrophilic infiltration occurred at 2-6 hours, followed by mononuclear infiltration at 6-24 hours.
- Endogenous PLA2 activity was detected in pleural exudate during RPAR-induced pleurisy, but its elevation lagged behind eicosanoid biosynthesis and plasma extravasation.
Conclusions:
- Exogenous PLA2 can induce pleural inflammation in rats.
- PLA2 is released endogenously during experimental pleurisy.
- The precise role of PLA2 in the inflammatory response warrants further investigation.