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Chemical Compound Review

Plicatic acid     (1S,2S,3R)-1-(3,4-dihydroxy- 5-methoxy...

Synonyms: SureCN452275, LS-117813, NSC 72234, BRN 2712741, AC1L2XL8, ...
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Disease relevance of NSC 72234

  • A rabbit model of hypersensitivity to plicatic acid, the agent responsible for red cedar asthma [1].
  • These observations suggest that plicatic acid could activate complement in vivo, thereby inducing an inflammatory response in the airways and contributing to the higher prevalence of industrial chronic bronchitis in exposed subjects [2].

High impact information on NSC 72234

  • Additionally, secoisolariciresinol dehydrogenase is involved in pathways to important plant defense molecules, such as plicatic acid in the western red cedar (Thuja plicata) heartwood [3].
  • Effect of plicatic acid on human serum complement includes interference with C1 inhibitor function [4].
  • OBJECTIVES: We sought to determine whether peripheral blood T cells from patients with western red cedar asthma (WRCA) recognize plicatic acid (PA) conjugated to human serum albumin (HSA) as judged by proliferation or cytokine production and to analyze the response to PA inhalation with flow cytometry [5].
  • T-lymphocyte responses to plicatic acid-human serum albumin conjugate in occupational asthma caused by western red cedar [5].
  • When the serum of PA-ovalbumin-sensitized guinea pigs was depleted of immunoglobulins and then used for passive sensitization of normal trachea, no contraction was observed when challenged with PA, suggesting that IgG1 antibodies mediate the tracheal reaction to PA.(ABSTRACT TRUNCATED AT 250 WORDS)[6]

Biological context of NSC 72234


Anatomical context of NSC 72234

  • 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 [11].
  • 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 [11].
  • Leukocyte chemotactic activity was also generated when serum was incubated with plicatic acid [2].
  • In conclusion, the late asthmatic reaction induced by plicatic acid in patients with western red cedar asthma is associated with an increase in sputum eosinophils [9].
  • In patients with asthma, a higher proportion of epithelial cells was observed in the 20 ml segmental bronchus lavage 24 to 48 hours after bronchial challenge with plicatic acid, the chemical compound responsible for red cedar asthma [12].

Associations of NSC 72234 with other chemical compounds

  • Activation of complement by plicatic acid was also confirmed by the demonstration of conversion of C3 to C3b on immunoelectrophoresis [2].
  • To characterize the mechanisms of PA-induced asthmatic reaction, guinea pigs were sensitized to PA through biweekly injection of PA-ovalbumin conjugate with aluminum hydroxide as an adjuvant for a period of 6 months [6].

Gene context of NSC 72234

  • Repeated inhalation challenge with plicatic acid in eight patients with LAR resulted in DAR in all [13].
  • At the first survey, workers completed a respiratory and occupational questionnaire, performed spirometry, gave serum for measurement of plicatic acid-specific IgE antibodies by radioallergosorbent testing, and had skin prick tests to detect atopy [14].

Analytical, diagnostic and therapeutic context of NSC 72234

  • In a cross-sectional survey of 652 workers in a western red-cedar sawmill, we obtained data on symptoms, pulmonary function, immediate skin reactivity to common allergens, nonspecific bronchial responsiveness, total IgE level, and sensitization to plicatic acid conjugated with human serum albumin as measured by RAST [15].
  • In order to investigate the relationship between the pattern of response (immediate, late and dual) to specific bronchial challenge test with plicatic acid or red cedar extract and the clinical features of asthma, 332 patients with asthma induced by western red cedar dust were examined at the time of diagnosis [16].


  1. A rabbit model of hypersensitivity to plicatic acid, the agent responsible for red cedar asthma. Chan, H., Tse, K.S., Van Oostdam, J., Moreno, R., Pare, P.D., Chan-Yeung, M. J. Allergy Clin. Immunol. (1987) [Pubmed]
  2. Activation of complement by plicatic acid, the chemical compound responsible for asthma due to western red cedar (Thuja plicata). Chan-Yeung, M., Giclas, P.C., Henson, P.M. J. Allergy Clin. Immunol. (1980) [Pubmed]
  3. Crystal structures of apo-form and binary/ternary complexes of Podophyllum secoisolariciresinol dehydrogenase, an enzyme involved in formation of health-protecting and plant defense lignans. Youn, B., Moinuddin, S.G., Davin, L.B., Lewis, N.G., Kang, C. J. Biol. Chem. (2005) [Pubmed]
  4. Effect of plicatic acid on human serum complement includes interference with C1 inhibitor function. Giclas, P.C. J. Immunol. (1982) [Pubmed]
  5. T-lymphocyte responses to plicatic acid-human serum albumin conjugate in occupational asthma caused by western red cedar. Frew, A., Chang, J.H., Chan, H., Quirce, S., Noertjojo, K., Keown, P., Chan-Yeung, M. J. Allergy Clin. Immunol. (1998) [Pubmed]
  6. Involvement of immunologic mechanisms in a guinea pig model of western red cedar asthma. Salari, H., Howard, S., Chan, H., Dryden, P., Chan-Yeung, M. J. Allergy Clin. Immunol. (1994) [Pubmed]
  7. Histamine and leukotrienes release in bronchoalveolar fluid during plicatic acid-induced bronchoconstriction. Chan-Yeung, M., Chan, H., Tse, K.S., Salari, H., Lam, S. J. Allergy Clin. Immunol. (1989) [Pubmed]
  8. Sensitivity and specificity of PC20 and peak expiratory flow rate in cedar asthma. Côté, J., Kennedy, S., Chan-Yeung, M. J. Allergy Clin. Immunol. (1990) [Pubmed]
  9. Sputum eosinophils and exhaled nitric oxide during late asthmatic reaction in patients with western red cedar asthma. Obata, H., Dittrick, M., Chan, H., Chan-Yeung, M. Eur. Respir. J. (1999) [Pubmed]
  10. Is specific antibody determination diagnostic for asthma attributable to low-molecular-weight agents? Weissman, D.N., Lewis, D.M. Occupational medicine (Philadelphia, Pa.) (2000) [Pubmed]
  11. Immunologic studies of the mechanisms of occupational asthma caused by western red cedar. Frew, A., Chan, H., Dryden, P., Salari, H., Lam, S., Chan-Yeung, M. J. Allergy Clin. Immunol. (1993) [Pubmed]
  12. Effect of bronchial lavage volume on cellular and protein recovery. Lam, S., Leriche, J.C., Kijek, K., Phillips, D. Chest (1985) [Pubmed]
  13. Relationship between types of asthmatic reaction, nonspecific bronchial reactivity, and specific IgE antibodies in patients with red cedar asthma. Lam, S., Tan, F., Chan, H., Chan-Yeung, M. J. Allergy Clin. Immunol. (1983) [Pubmed]
  14. A longitudinal study of the occurrence of bronchial hyperresponsiveness in western red cedar workers. Vedal, S., Enarson, D.A., Chan, H., Ochnio, J., Tse, K.S., Chan-Yeung, M. Am. Rev. Respir. Dis. (1988) [Pubmed]
  15. Plicatic acid-specific IgE and nonspecific bronchial hyperresponsiveness in western red-cedar workers. Vedal, S., Chan-Yeung, M., Enarson, D.A., Chan, H., Dorken, E., Tse, K.S. J. Allergy Clin. Immunol. (1986) [Pubmed]
  16. Pattern of specific airway response in asthma due to western red cedar (Thuja plicata): relationship with length of exposure and lung function measurements. Paggiaro, P.L., Chan Yeung, M. Clin. Allergy (1987) [Pubmed]
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