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Published on: December 19, 2013
Opposite effects of mast cell degranulation by compound 48/80 on peritoneal inflammation in Swiss and CBA mice
E Stankiewicz1, E Wypasek, B Plytycz
1Department of Evolutionary Immunology, Institute of Zoology, Jagiellonian University, Kraków, Poland.
Abstract:
The murine strains differ in the number of peritoneal mast cells. Degranulation of peritoneal mast cells by single injection of compound 48/80 (1.2 mg/kg) followed by zymosan-induced (2 mg/ml, 0.5 ml/mouse) peritoneal inflammation caused either inhibition or enhancement of an early influx (at 4 h of peritonitis) of exudatory leukocytes in Swiss and CBA mice, respectively. These opposite effects correspond with statistically significant differences in the number of peritoneal mast cells in the intact Swiss (11 x 10(3)) and CBA (39 x 10(3)) mice.
Insights
Murine strains exhibit varying peritoneal mast cell counts. Compound 48/80-induced mast cell degranulation oppositely affected leukocyte influx during zymosan-induced peritonitis in Swiss and CBA mice.
Area of Science:
- Immunology
- Cell Biology
Background:
- Murine strains possess distinct peritoneal mast cell populations.
- Peritoneal mast cells play a role in inflammatory responses.
Purpose of the Study:
- To investigate the differential effects of mast cell degranulation on leukocyte influx in two mouse strains.
- To correlate these effects with baseline mast cell numbers.
Main Methods:
- Compound 48/80 was used to induce mast cell degranulation.
- Zymosan-induced peritonitis was established in Swiss and CBA mice.
- Leukocyte influx into the peritoneal cavity was assessed at 4 hours.
Main Results:
- Swiss mice showed inhibited leukocyte influx post-degranulation.
- CBA mice exhibited enhanced leukocyte influx post-degranulation.
- Swiss mice had significantly fewer peritoneal mast cells (11 x 10^3) than CBA mice (39 x 10^3).
Conclusions:
- The number of peritoneal mast cells influences the inflammatory response to mast cell degranulation.
- Differential mast cell populations contribute to strain-specific inflammatory outcomes.

