Ara h 8, a Bet v 1–homologous allergen from peanut, is a major allergen in patients with combined birch pollen and peanut allergy

Mittag, Diana MSc
Akkerdaas, Jaap MSc
Ballmer-Weber, Barbara K. MD
Vogel, Lothar PhD
Wensing, Marjolein MD
Becker, Wolf-Meinhard PhD
Koppelman, Stef J. PhD
Knulst, André C. PhD
Helbling, Arthur MD
Hefle, Susan L. PhD
van Ree, Ronald PhD
Vieths, Stefan PhD

^aAllergy Unit, Department of Dermatology, University Hospital, Zurich, Switzerland
^bDepartment of Immunopathology, Sanquin, Amsterdam, The Netherlands
^cDepartment of Allergology, Paul-Ehrlich-Institut, Langen, Germany
^dDepartment of Dermatology/Allerogology, University Medical Center, Utrecht, The Netherlands
^eBiochemical and Molecular Allergology, Research Center, Borstel, Germany
^fTNO Nutrition and Food Research, Zeist, The Netherlands
^gDivision of Allergology, Department of Rheumatology, Clinical Immunology-Allergology, Inselspital, Bern, Switzerland
^hFood Allergy Research and Resource Program, University of Nebraska, Lincoln, Neb.

Reprint requests: Stefan Vieths, PhD, Department of Allergology, Paul-Ehrlich-Institut, D-63225 Langen, Germany. E-mail: [email protected].

^*These authors contributed equally to the study.

Supported by the 5th Framework Programme: Quality of Life and Management of Living Resources of the European Commission, QLK4-CT-2001-00301, and by the Swiss Federal Office for Education and Science, BBW 01.0159-1. Barbara Ballmer-Weber is a recipient of a grant from the Swiss National Foundation (Marie-Heim-Vögtlin, 32–66308.01). Also supported by a contribution of the University of Nebraska Agricultural Research Division, Lincoln, Nebraska, Journal Series No. 14544, and by a grant from the Allergy and Immunology Institute of the International Life Sciences Institute (ILSI) Research Foundation (Washington, DC). The opinions expressed herein are those of the authors and do not necessarily represent the views of ILSI.

Received for publication June 7, 2004; revised September 14, 2004; accepted for publication September 16, 2004.

Journal of Allergy & Clinical Immunology 114(6):p 1410-1417, December 2004.

Background

We recently described patients with soybean allergy mainly mediated by cross-reactivity to birch pollen allergens. A majority of those patients were reported to have peanut allergy.

Objective

We sought to study the occurrence of peanut allergy in patients allergic to birch pollen and characterized the Bet v 1–homologous peanut allergen Ara h 8.

Methods

Recombinant Ara h 8 was cloned with degenerated primers and expressed in Escherichia coli. Nine Swiss and 11 Dutch patients with peanut and birch pollen allergy and a positive double-blind, placebo-controlled food challenge result to peanut were investigated for IgE reactivity to birch pollen and purified peanut allergens and cross-reactivity between birch and peanut. Ara h 8 stability against digestion and roasting was assessed by means of RAST inhibition. The IgE cross-linking potency of Ara h 8 was tested on the basis of basophil histamine release.

Results

During double-blind, placebo-controlled food challenge, all patients experienced symptoms in the oral cavity, progressing to more severe symptoms in 40% of patients. CAP-FEIA detected recombinant (r) Ara h 8–specific IgE in 85%. IgE binding to Ara h 8 was inhibited by Bet v 1 in peanut extract immunoblotting and in RAST inhibition. In EAST inhibition recombinant rAra h 8 inhibited IgE binding to peanut in 4 of 7 tested patient sera. Antipeanut response was dominated by Ara h 8 in 12 of 17 tested patients. Furthermore, our results demonstrate a low stability of Ara h 8 to roasting and no stability to gastric digestion. Basophil histamine release with rAra h 8 was more than 20% in 5 of 7 tested sera.

Conclusions

Peanut allergy might be mediated in a subgroup of our patients by means of cross-reaction of Bet v 1 with the homologous peanut allergen Ara h 8.