Abstract
ObjectiveTo investigate whether eosinophilic bronchitis without airway hyperresponsiveness will develop bronchial asthma in allergic mice.MethodsMice were sensitized with OVA on days 0, 7, and 14, challenged on days 21 to 23 (1st OVA challenge), and re-challenged on days 46 to 48 (2nd OVA challenge), intranasally with 10 (the EB group) and 200 (the AS group) μg OVA. Lung resistance (RL) was assessed 24 h after each challenge and on day 45 followed by analysis of leukocyte distribution in the bronchoalveolar lavage (BAL) fluid and histological examination.ResultsTwenty-four hours after the 1st OVA challenge, aerosolized methacholine caused a dose-dependent increase in RL in all groups. At doses ≥1.56 mg/mL, RL in the AS group was significantly higher than that of the NS-1 group (P<0.01 or 0.05) and at doses ≥12.5 mg/mL, RL was markedly higher in the AS group than that of the EB group (P<0.01). The percentage of eosinophils in both the EB group and the AS group was markedly higher than that of the control group. Twenty-four hours after the 2nd OVA challenge, at doses ≤12.5 mg/mL, there was no significant difference in RL among all groups (P>0.05). At doses ≥12.5 mg/mL, RL in the AS group was significantly higher than that of the control group and EB group (P<0.01 or 0.05). The percentage of eosinophils in the AS group was noticeably higher than that of the EB group(P<0.05). Furthermore, there was apparent infiltration by inflammatory cells, predominantly eosinophils, into the sub-epithelial region of the bronchus and the bronchioles and around the vessels in the EB and AS group.ConclusionRe-challenge with low doses of ovalbumin did not increase airway reactivity and failed to induce bronchial asthma in mice with ovalbumin-induced EB.
Highlights
In 1989, Gibson et al first described a particular group of patients who had chronic irritating dry coughs with scant sputum with increased numbers of eosinophils in induced sputum
We investigated whether mice with ovalbumin (OVA)-induced eosinophilic bronchitis developed into asthma and further characterized the relation between eosinophilic bronchitis and asthma by using mouse models of OVA-induced eosinophilic bronchitis and asthma
We sensitized mice by intraperitoneal injection of 10 μg OVA followed by intranasal challenge with 10 μg OVA to establish a mouse model of eosinophilic bronchitis
Summary
In 1989, Gibson et al first described a particular group of patients who had chronic irritating dry coughs with scant sputum with increased numbers of eosinophils in induced sputum. These patients had normal ventilatory function with no airway hyperresponsiveness and had normal peak flow velocity rate. These patients responded well to glucocorticoid therapy. Park et al followed up 24 cases of eosinophilic bronchitis who were treated with inhalational glucocorticoids and they found that only one patient developed asthma over the two-year follow up [3].
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