Mechanisms of allergy and clinical immunology
Impaired allergy diagnostics among parasite-infected patients caused by IgE antibodies to the carbohydrate epitope galactose-α1,3-galactose

https://doi.org/10.1016/j.jaci.2011.01.033Get rights and content

Background

The carbohydrate epitope galactose-α1,3-galactose (α-Gal) is abundantly expressed on nonprimate mammalian proteins. We have recently shown that α-Gal is responsible for the IgE binding to cat IgA, a newly identified cat allergen (Fel d 5).

Objective

We sought to investigate the diagnostic relevance of IgE antibodies to Fel d 5 and α-Gal among parasite-infected patients from central Africa without cat allergy compared with patients with cat allergy from the same region.

Methods

Sera from 47 parasite-infected patients and 31 patients with cat allergy were analyzed for total IgE and IgE antibodies against cat dander extract (CDE) by using the ImmunoCAP system. Inhibition assay was performed with α-Gal on solid phase–bound CDE. The presence of IgE specific for the major cat allergen Fel d 1, Fel d 5, and α-Gal was analyzed by means of ELISA.

Results

Among the 47 parasite-infected patients, 85% had IgE antibodies against α-Gal (OD; median, 0.175; range, 0.102-1.466) and 66% against Fel d 5 (OD; median, 0.13; range, 0.103-1.285). Twenty-four of the parasite-infected patients were sensitized to CDE, and 21 of them had IgE antibodies to Fel d 5 and α-Gal. There was no correlation between IgE levels to CDE and rFel d 1 among the parasite-infected patients but a strong correlation between CDE and Fel d 5 and α-Gal (P < .001). Among the group with cat allergy, only 5 patients had IgE to α-Gal, and nearly 75% (n = 23) had IgE to rFel d 1 (median, 7.07 kUA/L; range, 0.51-148.5 kUA/L). In contrast, among the patients with cat allergy, there was a correlation between IgE levels to CDE and rFel d 1 (P < .05) but no correlation between CDE and Fel d 5 and α-Gal.

Conclusion

IgE to α-Gal causes impaired allergy diagnostics in parasite-infected patients. Screening for IgE to rFel d 1 and other allergens without carbohydrates might identify patients with true cat sensitization/allergy in parasite-infested areas.

Section snippets

Study subjects

Sera from a group of parasite-infected patients (n = 47) originating from rural Zimbabwe were included. The patients were given a diagnosis by a physician as being infected with schistosomiasis (n = 20), geohelminth infection (n = 16), or a combination (n = 11). The parasites causing geohelminth infection were Ascaris lumbricoides and Trichuris trichiura, along with the hookworms Necator americanus and Ancylostoma duodenale. The patients did not have a case history of cat allergy.

In addition,

Total IgE

There were no differences in total IgE levels between patients with cat allergy (median, 200 kU/L; range, 5-9,800 kU/L) and parasite-infected patients (median, 220 kU/L; range, 4.8-2,500 kU/L; P > .05) or between the various types of parasitic infections (P > .05, Fig 1).

Parasite-infected patients

Of the 47 patients in the parasite-infected group, 40 (85%) had IgE antibodies against α-Gal (OD; median, 0.175; range, 0.102-1.466), and 31 (66%) had IgE antibodies to Fel d 5 (OD; median, 0.13; range, 0.103-1.285). Notably,

Discussion

We here report that the majority of the 47 parasite-infected patients (85%) without reported symptoms of cat allergy from Zimbabwe have IgE antibodies against α-Gal, and 66% have IgE antibodies against Fel d 5. However, half of these patients were sensitized to CDE, and 21 of these 24 patients had IgE to Fel d 5, as well as to α-Gal. Furthermore, none of the CDE-sensitized patients had IgE to the major cat allergen rFel d 1. On the contrary, among the patients with cat allergy recruited from

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    Supported by the Swedish Research Council, the Swedish Asthma and Allergy Association's Research Foundation, the Swedish Heart-Lung Foundation, the Hesselman Foundation, the King Gustaf V 80th Birthday Foundation, the Konsul Th C Bergh Foundation, the Stockholm County Council, the Centre for Allergy Research at the Karolinska Institute, the Bernard Osher Initiative for Research on Severe Asthma, the Karolinska Institutet, the Austrian Science Fund, and the Christian Doppler Research Association.

    Disclosure of potential conflict of interest: R. Valenta has received research support from IWF (Austrian Science Fund), the Christian Doppler Research Association, Biomay, and Phadia and has consulted for Biomay and Phadia. M. van Hage has received research support from the Swedish Research Council, the Stockholm County Council, and the Swedish Asthma and Allergy Association’s Research Foundation. The rest of the authors have declared that they have no conflict of interest.

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