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Updated: Apr 21, 2026
Identification and Characterization of Immunogenic RNA Species in HDM Allergens that Modulate Eosinophilic Lung Inflammation
Published on: May 30, 2020
Lipopolysaccharide amplifies eosinophilic inflammation after segmental challenge with house dust mite in asthmatics
M Berger1, J D de Boer, P Bresser
1Department of Respiratory Medicine, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands; Department of Respiratory Medicine, Spaarne Hospital, Hoofddorp, The Netherlands.
Background:
House dust contains mite allergens as well as bacterial products such as lipopolysaccharide (LPS). Asthma exacerbations are associated with the level of exposure to allergens and LPS. LPS can potentiate allergen effects in steroid-naïve patients. Long-acting β2-agonists (LABA) were shown to inhibit LPS-induced bronchial inflammation in healthy volunteers. The aim of this study was to assess the effect of LPS on the allergen-induced eosinophilic inflammation [primary endpoints: eosinophil counts and eosinophil cationic protein (ECP)] induced by bronchial instillation of house dust mite (HDM) in patients with asthma on maintenance treatment with inhaled corticosteroids (ICS).
Methods:
Thirty-two nonsmoking asthmatics with HDM allergy were treated with run-in medication (fluticasone propionate 100 μg bid) during 2 weeks before the study day. All patients underwent bronchial challenge with HDM, and half of them were randomized to receive additional LPS. Both groups were randomized to receive pretreatment with a single inhalation of 100 μg salmeterol 30 min before bronchial segmental challenge. Six hours later, bronchoalveolar lavage (BAL) was collected for leukocyte cell count, differentials, and cellular activation markers.
Results:
Challenge with HDM/LPS induced a significant increase in eosinophil cationic protein (P = 0.036) and a trend toward an increase in BALF eosinophils as compared to HDM challenge.
Conclusion:
Lipopolysaccharide promotes eosinophilic airway inflammation in patients with asthma despite being on maintenance treatment with ICS.
Insights
Lipopolysaccharide (LPS) exposure exacerbates eosinophilic airway inflammation in asthma patients, even those on inhaled corticosteroid (ICS) maintenance therapy. This highlights LPS as a significant factor in asthma exacerbations.
Area of Science:
- Allergy and Immunology
- Respiratory Medicine
- Pharmacology
Background:
- House dust contains mite allergens and bacterial lipopolysaccharide (LPS).
- Asthma exacerbations correlate with exposure to allergens and LPS.
- LPS can amplify allergen effects in patients not using steroids.
Purpose of the Study:
- To evaluate LPS's impact on allergen-induced eosinophilic inflammation in asthma patients on inhaled corticosteroids (ICS).
- Primary endpoints included eosinophil counts and eosinophil cationic protein (ECP).
Main Methods:
- 32 asthma patients with HDM allergy received fluticasone propionate (100 μg bid) for 2 weeks.
- Patients underwent bronchial challenge with HDM, with half receiving additional LPS.
- Salmeterol pretreatment was administered before bronchial challenge; bronchoalveolar lavage (BAL) was collected 6 hours later.
Main Results:
- HDM/LPS challenge significantly increased eosinophil cationic protein (P = 0.036).
- A trend towards increased BALF eosinophils was observed compared to HDM challenge alone.
Conclusions:
- Lipopolysaccharide promotes eosinophilic airway inflammation in asthma patients.
- This occurs despite patients being on maintenance inhaled corticosteroid (ICS) treatment.
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