Several lines of evidence document a critical role for mast cells in
immune complex-mediated inflammatory models. However, their role in nonimmune models of acute
inflammation is largely unknown. In the present investigation, the role of mast cells was examined in
calcium ionophore (A23187)-induced mouse peritoneal
inflammation.
Intraperitoneal injection of
A23187 (20) micrograms/mouse) elicited marked and transient increases in immunoreactive levels of 6-ketoprostaglandin-F2 alpha,
leukotrienes B4, C4, D4, E4, and F4. There were no discernible differences in levels of these mediators in male Swiss Webster mice, mast cell-deficient mice (WBB6F1-W/W'), and age-matched controls (WBB6F1-+/+), suggesting a minimal role of mast cells in
eicosanoid biosynthesis in this model. However W/W' mice showed smaller increases in levels of
myeloperoxidase, a marker for neutrophils, compared to +/+ mice. Both W/W' and +/+ mice have lower constitutive levels of peritoneal
N-acetyl-beta-D-glucosaminidase (NAG), a marker for mononuclear cells. Similar to the changes seen in
myeloperoxidase, W/W' mice exhibited a blunted NAG response compared to +/+ mice. These results suggest that mast cell products other than
eicosanoids may contribute to the changes in cellular trafficking in response to intraperitoneal
A23187. These results also suggest that mast cells are required for full expression of inflammatory responses.