Background: Mites are the most common aeroallergen in human allergic asthma. However, no animal model of mite-induced allergic airway inflammation has been reported before. In this study, an animal model of mite-induced allergic airway inflammation in guinea pigs was developed. Methods: Firstly, we found that two intraperitoneal injections of 100 μg crude mite extract (CME), but not multiple aerosol inhalations of 10 mg/ml CME, can cause sensitization in guinea pigs. The sensitization to mites was confirmed by the measurement of serum antimite antibody titer and the detection of anaphylactic bronchoconstriction after intravenous injection of CME solution. Then, single or multiple aerosol challenges with different concentrations (8, 4 or 1 mg/ml) of CME in these sensitized animals were performed. The total white cell and differential counts in the bronchoalveolar lavage (BAL) fluids were studied at different time intervals after challenge in different animals, and tracheal pathology was performed to detect the allergic airway inflammation. For comparison with the study in animals treated with CME, a BAL study in animals treated with ovalbumin was also performed. Results: The inhalation challenge of CME aerosol in sensitized animals caused prolonged eosinophilia in BAL fluid which persisted for at least 7 days after single challenge. Neither inhalation challenge at higher concentrations of CME aerosol nor repeated inhalation challenges increased the degree of eosinophilia in BAL fluid compared to a single challenge. Using the same procedures, we also found that the mite model caused more eosinophilia in BAL fluid than did ovalbumin. Conclusion: This is the first report of an animal model of mite-induced allergic airway inflammation in guinea pigs which can provide us with a useful model to study airway inflammation of mite-induced asthma in humans.

Background: It is well known that eosinophilic airway inflammation develops after allergen challenge in sensitized humans and animals. However, the detailed time course of suppression of early eosinophilic airway inflammation by pharmacological agents given just after challenge has not been discussed. Therefore, we aimed to evaluate the time course relationship of the suppression of peak eosinophilia by anti–cytokines and pharmacological agents given several hours after the aerosol challenge by a therapeutic approach. Methods: We used crude mite extract as an allergen to create a sensitization and inhalation challenge, and performed bronchoalveolar lavages (BAL) after the inhalation challenge to observe the degree of eosinophilic airway inflammation in guinea pigs. Various anti–cytokines (anti–IL–3 and anti–IL–5) and pharmacological agents (dexamethasone, theophylline, and roxithromycin) were given within several hours after the acute aeorosol challenge to evaluate the suppressive effect on peak eosinophilia in BAL fluid, which occurred 24 h after the challenge. Results: Our results show that anti–IL–5 and dexamethasone, given within 4 and 8 h after the inhalation challenge, respectively, inhibit the acute allergen–induced peak eosinophilia in BAL fluid. However, anti–IL–3, theophylline, and roxithromycin had no effect on peak eosinophilic airway inflammation after challenge. Conclusion: These observations suggest that several hours are needed to complete the process of cytokine–induced recruitment of eosinophils from the blood to the airways after acute allergen challenge. This may be the optimal time to administer anti–cytokines and dexamethasone to attenuate the subsequent eosinophilic airway inflammation after acute allergen–induced asthmatic attacks.