Immunologic studies of the mechanisms of occupational asthma caused by western red cedar.

BACKGROUND Occupational asthma caused by western red cedar (Thuja plicata) is a common problem in sawmill industries. The objective of this study was to examine the cellular and immunologic mechanisms of western red cedar asthma (WRCA) more closely. METHODS Bronchial biopsy specimens, bronchoalveolar lavage (BAL) mast cells and peripheral blood basophils from patients with WRCA, patients with atopic asthma, and nonatopic control subjects were challenged in vitro with plicatic acid (PA), PA-human serum albumin conjugate (PA-HSA), grass pollen, or calcium ionophore. RESULTS PA (100 micrograms/ml) released histamine from the basophils of 9 of 11 patients with WRCA, 1 of 7 patients with atopic asthma, and 2 of 7 normal subjects. PA triggered histamine release from 10 of 11 bronchial biopsy specimens and 8 of 8 BAL samples from patients with WRCA. Interestingly, PA released histamine from BAL cells and bronchial biopsy specimens from 3 of 7 normal subjects but in none of the patients with atopic asthma. PA-HSA-induced histamine release from basophils and biopsy specimens was confined to patients with WRCA. PA-specific IgE was not detectable in serum from most patients with WRCA, and their serum did not transfer PA sensitivity to human lung fragments or lactate-stripped basophils. After pretreatment with anti-IgE in the absence of calcium, basophils from 14 subjects with WRCA still responded to PA (mean 64% to 67% of pretreatment response), whereas responses to grass pollen or anti-IgE were abolished. CONCLUSIONS This study confirms that PA releases histamine from bronchial mast cells of most patients with WRCA but not from those of patients with atopic asthma. The PA response of some normal subjects suggests that PA may have both specific and nonspecific actions on mast cells and basophils, whereas the serologic studies indicate histamine release in WRCA cannot simply be attributed to PA-specific IgE.

[1]  K. Kajiwara,et al.  Enhancement of IgE synthesis and histamine release by T cell factors derived from atopic patients with bronchial asthma. , 1987, The Journal of allergy and clinical immunology.

[2]  M. Chan-yeung,et al.  Bronchial reactions to western red cedar (Thuja plicata). , 1971, Canadian Medical Association journal.

[3]  E. Goetzl,et al.  Stimulation of histamine release from human basophils by human platelet factor 4. , 1983, The Journal of clinical investigation.

[4]  M. Chan-yeung,et al.  Natural history of occupational asthma: relevance of type of agent and other factors in the rate of development of symptoms in affected subjects. , 1992, The Journal of allergy and clinical immunology.

[5]  M. Chan-yeung Maximal expiratory flow and airway resistance during induced bronchoconstriction in patients with asthma due to Western red cedar (Thuja plicata). , 1973, The American review of respiratory disease.

[6]  E. Goetzl,et al.  A basophil-activating factor from human T lymphocytes. , 1984, Immunology.

[7]  A. Wardlaw,et al.  Morphological and secretory properties of bronchoalveolar lavage mast cells in respiratory diseases , 1986, Clinical allergy.

[8]  R. Alam,et al.  Histamine-releasing factors and inhibitors: historical perspectives and possible implications in human illness. , 1991, The Journal of allergy and clinical immunology.

[9]  A. Togias,et al.  Role of human basophils and mast cells in the pathogenesis of allergic diseases. , 1985, The Journal of allergy and clinical immunology.

[10]  A. Kay,et al.  Heterogeneous ultrastructure of human bronchial mast cells: morphometric subdivision of cell types and evidence for a degranulation gradient. , 1990, American journal of respiratory cell and molecular biology.

[11]  J. Balmes,et al.  Airway inflammation and occupational asthma. , 1988, Clinics in chest medicine.

[12]  R. Alam,et al.  A mononuclear cell derived histamine releasing factor (HRF) in asthmatic patients. Histamine release from basophils in vitro. , 1984, Annals of allergy.

[13]  M. Chan-yeung,et al.  Histamine and leukotrienes release in bronchoalveolar fluid during plicatic acid-induced bronchoconstriction. , 1989, The Journal of allergy and clinical immunology.

[14]  W. Boyle AN EXTENSION OF THE51Cr-RELEASE ASSAY FOR THE ESTIMATION OF MOUSE CYTOTOXINS , 1968, Transplantation.

[15]  J. Malo,et al.  Specific serum antibodies against isocyanates: association with occupational asthma. , 1989, The Journal of allergy and clinical immunology.

[16]  M. Chan-yeung,et al.  Immunologic and nonimmunologic mechanisms in asthma due to western red cedar (Thuja plicata). , 1982, The Journal of allergy and clinical immunology.

[17]  R. Patterson,et al.  Dissociation of IgE from receptors on human basophils. I. Enhanced passive sensitization for histamine release. , 1983, Journal of immunology.

[18]  A. Kagey‐Sobotka,et al.  Basophil histamine release induced by a substance from stimulated human platelets. , 1986, Journal of immunology.

[19]  L. Lichtenstein,et al.  Basic characteristics of human lung mast cell desensitization. , 1987, Journal of immunology.

[20]  J. Warner,et al.  Recombinant human IL-1 alpha and -1 beta potentiate IgE-mediated histamine release from human basophils. , 1989, Journal of immunology.

[21]  J. A. Grant,et al.  Histamine-releasing activity (HRA). I. Production by mitogen- or antigen-stimulated human mononuclear cells. , 1979, Journal of immunology.

[22]  M. Chan-yeung,et al.  Specific IgE antibodies in workers with occupational asthma due to western red cedar , 1982, Clinical allergy.

[23]  M. Kaliner,et al.  Neutrophils and mast cells. I. Human neutrophil-derived histamine-releasing activity. , 1987, Journal of immunology.

[24]  D. Cockcroft MECHANISM OF PERENNIAL ALLERGIC ASTHMA , 1983, The Lancet.

[25]  M. Chan-yeung,et al.  Clinical features and natural history of occupational asthma due to western red cedar (Thuja plicata). , 1982, The American journal of medicine.

[26]  Y. Alarie,et al.  Antigens which detect IgE antibodies in workers sensitive to toluene diisocyanate , 1980, Clinical allergy.

[27]  L. Lichtenstein,et al.  Generation of slow reacting substance by human leukocytes. II. Comparison of stimulation by antigen, anti-IgE, calcium ionophore, and C5-peptide. , 1980, Journal of immunology.

[28]  A. Notkins,et al.  Enhancement of IgE-mediated histamine release from human basophils by viruses: role of interferon , 1977, The Journal of experimental medicine.

[29]  R. Bowsher,et al.  A new radioenzymatic assay for histamine using purified histamine N-methyltransferase. , 1983, Life sciences.

[30]  A. Fauci,et al.  A histamine-releasing factor from activated human mononuclear cells. , 1985, Journal of immunology.

[31]  R. Alam,et al.  Comparative effect of recombinant IL-1, -2, -3, -4, and -6, IFN-gamma, granulocyte-macrophage-colony-stimulating factor, tumor necrosis factor-alpha, and histamine-releasing factors on the secretion of histamine from basophils. , 1989, Journal of immunology.

[32]  N. Johnson,et al.  Bronchoalveolar mast cells in extrinsic asthma: a mechanism for the initiation of antigen specific bronchoconstriction. , 1985, British medical journal.

[33]  V. Duronio,et al.  Characterization of platelet-activating factor receptors in porcine platelets. , 1990, Canadian Journal of Physiology and Pharmacology.

[34]  M. Chan-yeung,et al.  Relationship between types of asthmatic reaction, nonspecific bronchial reactivity, and specific IgE antibodies in patients with red cedar asthma. , 1983, The Journal of allergy and clinical immunology.