Interaction between hyperosmolar and IgE-mediated histamine release from basophils and mast cells.

Because both hyperosmolar and IgE-dependent stimuli may be encountered in the airway, and because hyperosmolarity causes histamine release in basophils, we examined the effects of the 2 stimuli on human lung mast cells. Mast cells prepared by enzymatic digestion of human lung were suspended in buffers made hyperosmolar with mannitol. Significant histamine release was seen above 360 mOsm/kg H2O, increasing to 11.9 +/- 1.0% at 770 mOsm/kg H2O, and release was synergistically enhanced by anti-IgE. Cells that had been rendered unresponsive to IgE-dependent stimuli by exposure to anti-IgE in the absence of Ca++ became markedly more responsive to hyperosmolar stimulation, and released as much as 32 +/- 2% histamine in hyperosmolar buffers alone. Antigen-induced histamine release from the basophils of allergic donors was also synergistically enhanced in buffers above 460 mOsm/kg H2O. These data show that immunologic and nonimmunologic stimuli may interact, and that human lung mast cells are capable of mediator release when exposed to osmolarities that may occur in the airway, especially during hyperventilation. Hyperosmolar mediator release is a plausible mechanism by which exercise-induced hyperventilation might induce asthma.

[1]  R. Naclerio,et al.  Mediator release after nasal airway challenge with allergen. , 2015, The American review of respiratory disease.

[2]  J. Fink,et al.  Food-dependent exercise-induced anaphylaxis. , 1983, The Journal of allergy and clinical immunology.

[3]  M. Walport,et al.  Exercise-induced release of histamine and neutrophil chemotactic factor in atopic asthmatics. , 1982, The Journal of allergy and clinical immunology.

[4]  L. Lichtenstein,et al.  Release of histamine from human leukocytes stimulated with the tumor-promoting phorbol diesters. II. Interaction with other stimuli. , 1982, Journal of immunology.

[5]  W. Hook,et al.  Influence of anions, cations and osmolarity on IgE-mediated histamine release from human basophils. , 1981, Immunology.

[6]  A. Kagey‐Sobotka,et al.  Hyperosmolar triggering of histamine release from human basophils. , 1981, The Journal of clinical investigation.

[7]  J. Gatzy,et al.  Regional differences in airway surface liquid composition. , 1981, Journal of applied physiology: respiratory, environmental and exercise physiology.

[8]  E. R. Mcfadden,et al.  Magnitude and site of airway response to exercise in asthmatics in relation to arterial histamine levels. , 1980, The Journal of allergy and clinical immunology.

[9]  E. R. Mcfadden,et al.  Evaluation of role played by mediators of immediate hypersensitivity in exercise-induced asthma. , 1980, The Journal of clinical investigation.

[10]  L. Lichtenstein,et al.  In vitro studies of antigen-induced bronchospasm: effect of antihistamine and SRS-A antagonist on response of sensitized guinea pig and human airways to antigen. , 1979, Journal of immunology.

[11]  G. K. Adams,et al.  Effects of temperature, relative humidity, and mode of breathing on canine airway secretions. , 1979, Journal of applied physiology: respiratory, environmental and exercise physiology.

[12]  P. Paré,et al.  The number and distribution of mast cells in monkey lungs. , 1979, The American review of respiratory disease.

[13]  E. R. Mcfadden,et al.  Influence of heat and humidity on the airway obstruction induced by exercise in asthma. , 1978, The Journal of clinical investigation.

[14]  J. Hendley,et al.  Histamine in nasal secretions. , 1978, International archives of allergy and applied immunology.

[15]  R. Patterson,et al.  Reagin-mediated asthma in rhesus monkeys and relation to bronchial cell histamine release and airway reactivity to carbocholine. , 1976, The Journal of clinical investigation.

[16]  P. Eggleston.  Exercise-induced asthma in children with intrinsic and extrinsic asthma. , 1975, Pediatrics.

[17]  H. Gilbert,et al.  Basophil counting with a new staining method using alcian blue. , 1975, Blood.

[18]  K.,et al.  FORMATION OF SLOW-REACTING SUBSTANCE OF ANAPHYLAXIS IN HUMAN LUNG TISSUE AND CELLS BEFORE RELEASE , 1974, The Journal of experimental medicine.

[19]  R. Siraganian.  An automated continuous-flow system for the extraction and fluorometric analysis of histamine. , 1974, Analytical biochemistry.

[20]  R. Patterson,et al.  Respiratory mast cells and basophiloid cells. I. Evidence that they are secreted into the bronchial lumen, morphology, degranulation and histamine release. , 1974, Clinical and experimental immunology.

[21]  R. Case,et al.  The relationship between calcium exchange and enzyme secretion in the isolated rat pancreas , 1973, The Journal of physiology.

[22]  H. Harving,et al.  The relationship between the transport of glucose and cations across cell membranes in isolated tissues. 8. The effect of membrane stabilizers on the transport of K + , Na + and glucose in muscle, adipocytes and erythrocytes. , 1973, Biochimica et biophysica acta.

[23]  D. Gómez,et al.  Respiratory heat exchange in normal subjects and in patients with pulmonary disease. , 1969, Journal of applied physiology.

[24]  J. L. Potter,et al.  Studies on pulmonary secretions. II. Osmolality and the ionic environment of pulmonary secretions from patients with cystic fibrosis, bronchiectasis, and laryngectomy. , 1967, The American review of respiratory disease.

[25]  A. G. Osler,et al.  STUDIES ON THE MECHANISMS OF HYPERSENSITIVITY PHENOMENA. IX. HISTAMINE RELEASE FROM HUMAN LEUKOCYTES BY RAGWEED POLLEN ANTIGEN. , 1964 .