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Clinical & Experimental Allergy

Lack of role for mononuclear cell-derived histamine releasing factors in occupational asthma due to western red cedar

Authors

  • A. J. FREW,

    Corresponding author
    1. Canadian Network of Centres of Excellence. Respiratory Health, Respiratory Division, Department of Medicine Vancouver General Hospital, University of British Columbia. Vancouver, Canada
      Dr A. J. Frew, University Medicine, Southampton General Hospital. Southampton, S094XY. U.K.
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  • H. CHAN,

    1. Canadian Network of Centres of Excellence. Respiratory Health, Respiratory Division, Department of Medicine Vancouver General Hospital, University of British Columbia. Vancouver, Canada
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  • M. CHAN YEUNG

    1. Canadian Network of Centres of Excellence. Respiratory Health, Respiratory Division, Department of Medicine Vancouver General Hospital, University of British Columbia. Vancouver, Canada
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Dr A. J. Frew, University Medicine, Southampton General Hospital. Southampton, S094XY. U.K.

Summary

Occupational asthma due to Western Red Cedar (WRCA) is attributed to sensitization to plicatic acid (PA), but does not appear to be dependent on PA-specific IgE antibodies. Exposure to PA induces histamine release in vivo and in vitro, so if IgE is not important. other mechanisms of histamine release must presumably operate in WRCA, To explore the possible role of histamine-releasing factors in WRCA, peripheral blood mono-nuclear cells were obtained and cultured with PA, PA-albumin conjugate plica tic acid-human serum albumin (PA-HSA).grass pollen or Concanavalin A using a standard histamine releasing factor (HRF) generation protocol. Supernatants were dialysed to remove endogenous histamine and then assayed for histamine releasing activity using human basophils as targets and a Con A-induced bulk supernatant as an internal HRF standard. In contrast to some previous reports, spontaneous HRF release from the peripheral blood mononuclear cells (PBMC) of WRCA patients (n= 9) and atopic asthmatic subjects (n= 5) was not elevated compared with the non-asthmatic controls (n= 11; five atopic and six non-atopic). Both PA and PA-HSA induced the production of small amounts of HRF by PBMC of WRCA patients, but a similar degree of HRF generation was also observed in PBMC from the atopic asthmatic, atopic non-aslhmatic, and non-atopic subjects. The contrast, grass pollen induced the production of HRF by PBMC from the subjects with positive skin tests to grass pollen but not by PBMC of non-atopic subjects, confirming that our methods and assay were capable of detecting antigen-specific HRF production. Since neither PA nor PA-HSA induced significantly elevated HRF production from PBMC of WRCA patients, it seems unlikely that PA-induced HRFs play a substantial role in the pathogenesis of WRCA.

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