Abstract
In the airway, gastrointestinal tract, renal parenchyma, and during some clinical situations, basophils and mast cells are exposed to a hyperosmolar milieu. We have shown that hyperosmolar stimuli release pharmacologically active mediators and that the process is distinct from IgE-dependent release. Significant mast cell histamine release occurs at just above physiologic levels (360 mOsm) and reaches a maximum of 12±1% at 770 mOsm; release from basophils is significant at 560 mOsm and reaches a maximum of 45±7% at 1020 mOsm. Activation of mast cells is dependent on extracellular Ca++ but maximal release from basophils is only partially reduced in Ca++ free buffers. Hyperosmolar buffers also increase IgE-dependent histamine release synergistically (mast cells: 460 mOsm 7±1% release; 1 μg/ml anti IgE 7±1%; both 27±4%). Prostaglandin D2 (PGD2) production from mast cells at 770 mOsm (69 pg/100 μ1) was not different from unstimulated cells (83 pg/100 μ1) despite significant histamine release (16% vs. 4% control). Furthermore, IgE-dependent PGD2 production (264 pg/100 μ1) was suppressed (99 pg/100 μ1) in hyperosmolar buffers (p<0.01). The distinctive activation by hyperosmolarity and its interaction with IgE-dependent activation may have important implications for airway physiology, and the management of radiocontrast anaphylactoid reactions and clinical hyperosmolarity syndromes.
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