What causes allergy to house dust and mites? - briefly
Allergenic proteins in house‑dust mite feces, body fragments, and related contaminants (e.g., mold spores, cockroach debris) are the main triggers. In sensitized individuals these proteins provoke an IgE‑mediated immune response, causing symptoms such as sneezing, itching, and airway inflammation.
What causes allergy to house dust and mites? - in detail
Allergic reactions to indoor dust and mites arise from exposure to specific protein fragments that the immune system mistakenly identifies as harmful. These proteins, known as allergens, are present in mite fecal pellets, body fragments, and secretions. The most potent allergens include Der p 1 and Der f 1 from the common house dust mite Dermatophagoides pteronyssinus and D. farinae, as well as group 2, 5, and 21 allergens that share similar structures. Additional contributors are proteins from storage mites, cockroach debris, mold spores, pet dander, and pollen that often embed in settled dust.
When a susceptible individual inhales or contacts these particles, antigen‑presenting cells process the proteins and present them to T‑helper 2 (Th2) lymphocytes. The Th2 response drives B‑cell production of immunoglobulin E (IgE) specific to the dust‑mite allergens. IgE molecules bind to high‑affinity receptors on mast cells and basophils throughout the respiratory tract and skin. Subsequent exposure triggers cross‑linking of IgE on these cells, causing rapid release of histamine, leukotrienes, and cytokines. The resulting inflammation produces typical symptoms such as sneezing, rhinorrhea, itchy eyes, wheezing, and eczema.
Several factors modulate the intensity of sensitization:
- Environmental humidity: Relative humidity above 50 % promotes mite proliferation and fecal particle dispersion.
- Temperature: Warm indoor climates (20–25 °C) accelerate mite life cycles.
- Housing characteristics: Carpeting, upholstered furniture, and heavy bedding provide habitats and reservoirs for mites and dust.
- Ventilation: Poor air exchange allows accumulation of allergen‑laden particles.
- Genetic predisposition: Families with a history of atopy exhibit higher IgE responses to dust‑mite proteins.
- Early‑life exposure: Infants in heavily contaminated environments are more likely to develop sensitization, although some studies suggest that limited exposure may induce tolerance.
The immune cascade can be amplified by co‑sensitization to other indoor allergens, such as cockroach or mold proteins, which share epitopic similarity with mite allergens. This cross‑reactivity broadens the spectrum of triggers and can worsen clinical outcomes.
Preventive measures target the reduction of allergen load and the interruption of immune activation. Strategies include maintaining humidity below 45 %, using allergen‑impermeable mattress and pillow encasements, washing bedding at ≥60 °C weekly, removing wall‑to‑wall carpeting, and employing high‑efficiency particulate air (HEPA) filtration. In cases of established sensitization, pharmacologic interventions (antihistamines, intranasal corticosteroids) and immunotherapy aim to diminish IgE‑mediated responses.