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and Granulocyte-Macrophage Colony-Stimulating Factor1
*
Department of Pharmacology, School of Pharmacy, The Hebrew University-Hadassah Medical School, Jerusalem, Israel; and
David R. Bloom Center of Pharmacy
Mast cell-eosinophil interactions in allergy have not yet been
completely defined. To determine whether mast cells influence
eosinophil survival, human peripheral blood eosinophils were incubated
with rat peritoneal mast cell sonicate. After 3 days, viable
eosinophils in medium were 21.3% compared with 44% with mast cell
sonicate. Like sonicate, supernatants of compound 48/80-activated mast
cells enhanced eosinophil survival, demonstrating that the factor(s)
involved is stored preformed and rapidly released. Increased eosinophil
survival was due to an inhibition of apoptosis (morphologic analysis;
annexin V/PI). Neutralizing Abs to granulocyte-macrophage CSF (GM-CSF),
but not to IL-3 or IL-5, decreased by 61.7% the enhancing effect on
eosinophil viability. Eosinophils are the source of GM-CSF since its
release in the culture medium was inhibited by their incubation with
the mast cell sonicate together with dexamethasone. In addition,
eosinophils incubated with the sonicate expressed mRNA for GM-CSF. To
partially characterize the mast cell-derived factor(s) increasing
eosinophil survival, the sonicate was heated (56°C/30 min or
100°C/10 min) or preincubated with antihistamines or with
anti-TNF-
-neutralizing Abs. Most of the activity was heat
labile. TNF- was found to be predominantly (70%) responsible, while
histamine had no role. Mast cell sonicate also caused eosinophils to
release eosinophil peroxidase and to display morphologic signs of
activation. In conclusion, we have demonstrated that mast cells enhance
eosinophil survival in part through their activation to produce and
release the autocrine survival cytokine GM-CSF.
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