The relevance of microbial allergens to the IgE antibody repertoire in atopic and nonatopic eczema.
BACKGROUND
A propensity to microbial skin infections has been reported in atopic ("high IgE") and nonatopic ("low IgE") forms of eczema. However, the relationship between antimicrobial IgE antibodies and nonatopic disease is unclear.


OBJECTIVE
We examined the relevance of microbial allergens to the allergen-specific IgE antibody repertoire in patients with atopic dermatitis.


METHODS
Patients with IgE levels of less than 150 IU/mL were stratified according to sensitivity (n = 22) or no sensitivity (n = 27) to 11 common food allergens and aeroallergens. The prevalence and titers of antimicrobial IgE antibodies were compared with those of patients (n = 36) with increased total IgE levels (>150 IU/mL). Skin-derived serum chemokines were also analyzed.


RESULTS
Patients with low IgE levels showed decreased disease severity, increased age of onset, a striking female predominance, and a distinct distribution of skin lesions. High titer IgE antibodies (sum of 8 bacterial and fungal allergens = 29.8 +/- 32.6 IU/mL) and multisensitization specific for microbial allergens was characteristic of patients with high IgE levels, with an overall 84% positivity; however, antimicrobial IgE antibodies comprised 3% or less of allergen-specific IgE antibodies. By contrast, antimicrobial IgE antibodies were detected in only 20% of patients with low IgE, and titers were negligible, irrespective of sensitization to common allergens. These patients were monosensitized, and exclusive microbial sensitivity was uncommon (10%). Patients with low IgE with no sensitivity to common allergens had lower levels of serum macrophage inflammatory protein 3alpha compared with their sensitized counterparts.


CONCLUSIONS
Antimicrobial IgE antibodies are uncommon in patients with atopic dermatitis with low IgE levels.


CONCLUSIONS
Hypersensitivity to microbial allergens is an unlikely trigger for eczematous eruptions in patients with low IgE levels.
Reefer
Amanda J
AJ
Asthma and Allergic Diseases Center, University of Virginia Health System, Charlottesville, VA 22908-1355, USA.
Satinover
Shama M
SM
Wilson
Barbara B
BB
Woodfolk
Judith A
JA
D000328:Adult; D000485:Allergens / Q000276:immunology*; D000942:Antigens, Bacterial / Q000276:immunology*; D000946:Antigens, Fungal / Q000276:immunology*; D054418:Chemokine CCL20; D019742:Chemokines, CC / Q000097:blood; D003876:Dermatitis, Atopic / Q000175:diagnosis / Q000276:immunology*; D004485:Eczema / Q000175:diagnosis / Q000276:immunology*; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood* / Q000276:immunology; D019402:Macrophage Inflammatory Proteins / Q000097:blood; D008297:Male
D000485:Allergens; D000942:Antigens, Bacterial; D000946:Antigens, Fungal; C108355:CCL20 protein, human; D054418:Chemokine CCL20; D019742:Chemokines, CC; D019402:Macrophage Inflammatory Proteins; D007073:Immunoglobulin E