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Aspergillus niger (m207) IgE Test

The Aspergillus niger IgE test measures serum-specific IgE against the m207 allergen, detecting IgE-mediated sensitisation to this ubiquitous environmental mould. It is ordered to investigate respiratory allergy, allergic bronchopulmonary aspergillosis, and asthma exacerbations linked to damp indoor environments, interpreted alongside clinical history, total IgE, and imaging.

1

Biomarkers

Blood (serum)

Sample

3–5 business days

Turnaround

No

Fasting

What is the Aspergillus niger IgE test?

The Aspergillus niger IgE test detects serum-specific IgE against the m207 allergen, a common environmental mould. Practitioners order this test to investigate respiratory symptoms — chronic rhinitis, asthma exacerbations, persistent cough — in patients who report exposure to damp indoor environments, suspect mould allergy, or present with eosinophilia or radiographic infiltrates suggestive of allergic bronchopulmonary aspergillosis. In the diagnostic landscape it sits alongside skin prick testing, total IgE, precipitins (IgG antibodies), pulmonary function tests, and imaging. Skin testing offers higher sensitivity and immediate results, but serum IgE is preferred when antihistamines cannot be withheld, when dermatographism or extensive eczema precludes skin tests, or when the clinician needs a quantitative, standardised result for serial monitoring. The test does not diagnose invasive aspergillosis, which is driven by tissue invasion rather than IgE-mediated allergy.

What does the Aspergillus niger IgE test measure?

1
m207 IgE(Aspergillus niger-specific Immunoglobulin E)
Range: <0.10 kU/L (Class 0, undetectable). Class 1 (0.10–0.34) equivocal; Class 2–6 (≥0.35) positive with increasing likelihood of clinical sensitivity.Optimal: Class 0 (<0.10 kU/L) indicates no detectable sensitisation. Class 1 is equivocal and should be correlated with exposure history and symptoms; Class 2 and above carry progressively higher likelihood of clinical reactivity, though magnitude does not reliably predict symptom severity.kU/L / IU/mL

Aspergillus niger is a ubiquitous saprophytic fungus abundant in soil, decaying vegetation, and indoor environments with water damage or high humidity. Inhalation of airborne conidia triggers IgE synthesis in atopic individuals, with class-switched B cells producing allergen-specific IgE that binds high-affinity FcεRI receptors on mast cells and basophils. Upon re-exposure, cross-linking of surface IgE releases histamine, leukotrienes, and cytokines, mediating immediate hypersensitivity. Cross-reactivity among Aspergillus species (A. fumigatus, A. flavus, A. niger) is common, driven by shared antigens such as Asp f components.

Serum IgE to Aspergillus niger identifies IgE-mediated sensitivity in patients with suspected mould allergy, allergic rhinitis, allergic asthma, or allergic bronchopulmonary aspergillosis. A positive result does not establish clinical allergy by itself — sensitisation must correlate with history and symptoms. Elevated Aspergillus IgE is one element of the ABPA diagnostic criteria, though total IgE and A. fumigatus-specific IgE are typically more prominent. This test informs environmental remediation, helps distinguish sensitisation from active ABPA, and guides decisions about antifungal or immunomodulatory therapy.

Why is the Aspergillus niger IgE test ordered?

  • Evaluation of chronic rhinitis, conjunctivitis, or asthma in patients reporting symptoms worsened by damp, mouldy indoor environments or water-damaged buildings
  • Work-up of suspected allergic bronchopulmonary aspergillosis in asthma patients with eosinophilia, mucus plugging, or central bronchiectasis
  • Investigation of persistent respiratory symptoms in patients with known atopy and prior Aspergillus exposure, to stratify sensitisation status
  • Preoperative or pre-biologic assessment of mould sensitisation in severe asthma candidates for biologics targeting IgE or type-2 inflammation
  • Differentiation of IgE-mediated hypersensitivity from IgG-mediated extrinsic allergic alveolitis (hypersensitivity pneumonitis), where precipitins rather than IgE predominate
  • Monitoring of Aspergillus-sensitised patients after environmental remediation or during immunomodulatory therapy, when serial quantitative results inform response
  • Confirmation of sensitisation when skin prick testing is contraindicated, not tolerated, or yields equivocal results

Sample collection and turnaround

Sample type

Blood (serum)

Fasting required

No

Collection method

Venipuncture at patient service centre

Turnaround

3–5 business days

Collection notes

Phlebotomy at a Quest Diagnostics patient service centre; no special preparation. If the patient is on antihistamines, serum IgE is unaffected and remains valid, unlike skin prick testing. Note recent corticosteroid or biologic therapy in the clinical history, as this may suppress IgE synthesis.

Specimen requirements

Minimum 0.5 mL serum in a red-top or gel separator tube. Separate from cells and refrigerate or freeze if not assayed promptly. Specific IgE is stable frozen for extended periods.

What can affect Aspergillus niger IgE results?

elevatesCross-reactivity among Aspergillus species

Shared antigens among A. niger, A. fumigatus, and A. flavus can produce positive IgE results across multiple species; component-resolved diagnostics can clarify the primary sensitiser if clinically important.

elevatesTotal IgE and polyclonal B-cell activation

Markedly elevated total IgE (as in ABPA or parasitic infection) can raise the baseline of specific IgE assays, occasionally producing low-level positive results of uncertain clinical significance.

reducesRecent systemic corticosteroid or immunosuppressive therapy

High-dose corticosteroids or biologics such as omalizumab can suppress IgE synthesis and lower measured specific IgE, potentially masking true sensitisation if drawn during peak therapy.

variableSeasonal and indoor exposure variability

Aspergillus spore concentrations fluctuate with season and indoor humidity; IgE levels may rise after recent heavy exposure or fall during periods of avoidance, so timing relative to exposure influences results.

variableAge and natural history of atopy

IgE sensitisation patterns evolve with age — young children may show transient low-level positivity, while established sensitisation in adults tends to persist, though titre does not reliably track symptom severity.

What do Aspergillus niger IgE results mean?

Elevated

Class 2 and above (≥0.35 kU/L) indicates detectable IgE sensitisation to Aspergillus niger, consistent with IgE-mediated hypersensitivity. Correlate with clinical history — symptoms triggered by damp environments, positive skin test, peripheral eosinophilia, or ABPA criteria. Isolated sensitisation without symptoms does not require treatment; management focuses on allergen avoidance, inhaled corticosteroids, and consideration of antifungal or biologic therapy in ABPA.

Normal

Class 1 (0.10–0.34 kU/L) is equivocal and should be interpreted with caution. If symptoms and exposure history are compelling, consider repeat testing after interval exposure, skin prick testing, or component-resolved diagnostics to clarify clinical relevance.

Reduced

Class 0 (<0.10 kU/L) indicates no detectable IgE to Aspergillus niger and makes IgE-mediated mould allergy to this species unlikely. It does not exclude sensitisation to other moulds (Alternaria, Cladosporium, Penicillium), non-IgE mechanisms such as hypersensitivity pneumonitis, or clinical allergy mediated by other Aspergillus species if this organism was not the relevant exposure.

Note: Positive IgE indicates sensitisation, not disease. Asymptomatic sensitisation is common among atopic individuals with environmental exposure and does not mandate therapy. Conversely, negative IgE does not exclude non-IgE-mediated pulmonary disease or allergy to other mould species. In suspected ABPA, measure total IgE and Aspergillus fumigatus-specific IgE alongside A. niger, as A. fumigatus is the predominant species in most cases.

Frequently asked questions

Aspergillus niger is a common environmental mould found in soil, decaying vegetation, and water-damaged buildings. In atopic individuals, inhaled spores trigger IgE-mediated hypersensitivity, causing allergic rhinitis, asthma, or contributing to allergic bronchopulmonary aspergillosis.

How to access the Aspergillus niger IgE test

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About this page

Published: October 7, 2026

Last reviewed: October 7, 2026

References:
  1. Agarwal R, et al. Allergic bronchopulmonary aspergillosis: review of literature and proposal of new diagnostic and classification criteria. Clin Exp Allergy. (2013)
  2. Greenberger PA. Allergic bronchopulmonary aspergillosis. J Allergy Clin Immunol. (2002)
  3. Patterson K, et al. Interpretation of specific IgE testing in allergy diagnosis. Ann Allergy Asthma Immunol. (2018)
  4. Baxi SN, Phipatanakul W. The role of allergen exposure and avoidance in asthma. Adolesc Med State Art Rev. (2010)

This content is for licensed healthcare practitioners only and does not constitute medical advice. Clinical decisions should be based on the full clinical picture and not on any single test result.