The purpose of this study was to establish the animal model of chronic human asthma characterized by airway remodeling. During the course of making animal model, the author tried to elucidate the time sequence of airway hyperresponsiveness, airway inflammation, airway remodeling.
7-week-old female BALB/c mice were studied for chronic asthma model using ovalbumin(OVA), and they were divided 3 asthma groups depending on the duration of OVA inhalation(group I; 4 weeks, group II; 8 weeks, group III; 12 weeks) and a control group. Airway resistance was measured for airway hyperresponsiveness, serum total IgE, IgG1, IgG2a were measured. PAS and Masson’s trichrome stain in the lung tissue were measured.
1. Airway hyperresponsiveness was significantly increased in all asthma groups than control group. 2. Serum total IgE was significantly increased in all asthma groups, group I, group II, group III(0.99±0.30 μg/ml, 2.66±1.16 μg/ml, 2.42±0.92 μg/ml, respectively) than control group(0.41±0.16 μg/ml)(P<0.01). And among asthma groups, total IgE was significantly increased in group II and group III than group I(P<0.01). 3. OVA specific IgG1, IgG2a were not detected in control group. In asthma groups, OVA specific IgG1 was significantly increased in group II(9.58±0.13 A.U.) than group I(9.33±0.23 A.U.), and group III(11.22±1.51 A.U.) than group II(9.58±0.13 A.U.)(P<0.01). 4. In the lung tissue stained with PAS, goblet cell hyperplasia was significantly increased in all asthma groups than control group(P<0.01). 5. In the lung tissue stained with Masson’s trichrome, peribronchial fibrosis was increased in all asthma groups than control group(P<0.01). Among asthma groups, time dependent increase in peribronchial fibrosis was observed.
In this ovalbumin induced murine model, airway inflammation as well as airway hyperresponsiveness was sustained and airway remodeling was developed, so chronic asthma was achieved. In this process, the author thought that IgE, IgG1, IgG2a as well as inflammatory cells were continuously attributed for the pathogenesis of chronic asthma.
Chronic asthma model in mouse.
J. Kim, None.