The Journal of Allergy and Clinical Immunology
Volume 119, Issue 3 , Page 758, March 2007

Reply

  • Meinir Jones, PhD

      Affiliations

    • From the Department of Occupational and Environmental Medicine, National Heart and Lung Institute, Imperial College, London, United Kingdom
    • ,
  • Alison Floyd, BSc

      Affiliations

    • From the Department of Occupational and Environmental Medicine, National Heart and Lung Institute, Imperial College, London, United Kingdom
    • ,
  • Kayhan T. Nouri-Aria, FRCPath

      Affiliations

    • Department of Allergy and Clinical Immunology, National Heart and Lung Institute, Imperial College, South Kensington, United Kingdom
    • ,
  • Mikila R. Jacobson, PhD

      Affiliations

    • Department of Allergy and Clinical Immunology, National Heart and Lung Institute, Imperial College, South Kensington, United Kingdom
    • ,
  • Stephen R. Durham, MD

      Affiliations

    • Department of Allergy and Clinical Immunology, National Heart and Lung Institute, Imperial College, South Kensington, United Kingdom
    • ,
  • Anthony Newman Taylor, FRCP

      Affiliations

    • From the Department of Occupational and Environmental Medicine, National Heart and Lung Institute, Imperial College, London, United Kingdom
    • ,
  • Paul Cullinan, MD

      Affiliations

    • From the Department of Occupational and Environmental Medicine, National Heart and Lung Institute, Imperial College, London, United Kingdom

published online 25 January 2007.

Article Outline

 

To the Editor:

We appreciate Dr Baur's1 interest in our recent publication2 concerning IgE and asthma from diisocyanates. We reported an absence of Cε and IL-4 mRNA–positive cells in bronchial biopsy specimens taken from patients 24 hours after a challenge with diisocyanate. Dr Baur comments that Maestrelli et al3 found significantly increased IL-4 in the bronchial mucosa of isocyanate responders with asthma. This was the case 48 hours after active challenge but not at 1 to 4 weeks after the last workplace exposure. These authors commented that the increased expression of IL-4 after challenge was in contrast with their finding that only a minority of T-cell clones (6%) derived from bronchial mucosa had detectable IL-4. It is not clear from the published report whether the patients in that study had evidence of specific IgE sensitization.

Dr Baur is indeed correct in pointing out that IgE-mediated sensitization occurs in diisocyanate workers; as is widely acknowledged, such sensitization is only detected in about a quarter of patients with asthma from this cause. On this basis of our findings, we concluded that the disease might be IgE-independent in a proportion of patients. We further hypothesized that there may be 2 separate forms, one associated with IgE and the other not. We did not imply that diisocyanate asthma is a non–IgE-mediated disease in those patients with detectable specific IgE.

We hope that our study will now be repeated in a larger population of patients with diisocyanate asthma, including those with and without detectable specific IgE.

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References 

  1. Baur X. Evidence for allergic reactions in isocyanate asthma. J Allergy Clin Immunol. 2007;119:757–758
  2. Jones MG, Floyd A, Nouri-Aria KT, Jacobson MR, Durham SR, Newman Taylor A, et al. Is occupational asthma to diisocyanates a non-IgE-mediated disease?. J Allergy Clin Immunol. 2006;117:663–669
  3. Maestrelli P, Occari P, Turato G, Papiris SA, Di Stefano A, Mapp CE, et al. Expression of interleukin (IL)-4 and IL-5 proteins in asthma induced by toluene diisocyanate (TDI). Clin Exp Allergy. 1997;27:1292–1298

 Disclosure of potential conflict of interest: The authors have declared that they have no conflict of interest.

PII: S0091-6749(06)02347-5

doi:10.1016/j.jaci.2006.10.038

The Journal of Allergy and Clinical Immunology
Volume 119, Issue 3 , Page 758, March 2007

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