Re-challenge with ovalbumin failed to induce bronchial asthma in mice with eosinophilic bronchitis.
OBJECTIVE
To investigate whether eosinophilic bronchitis without airway hyperresponsiveness will develop bronchial asthma in allergic mice.


METHODS
Mice were sensitized with OVA on days 0, 7, and 14, challenged on days 21 to 23 (1(st) OVA challenge), and re-challenged on days 46 to 48 (2(nd) 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.


RESULTS
Twenty-four hours after the 1(st) 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 2(nd) 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.


CONCLUSIONS
Re-challenge with low doses of ovalbumin did not increase airway reactivity and failed to induce bronchial asthma in mice with ovalbumin-induced EB.
Department of Respiratory Medicine, the 1st Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China ; Guangzhou Institute of Respiratory Disease, Guangzhou, Guangdong, China ; State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, Guangdong, China.
Liyan
L
Chen
Nanshan
N
Zhong
Kefang
K
Lai
D000281:Administration, Intranasal; D000336:Aerosols / Q000008:administration & dosage; D000818:Animals; D001249:Asthma / Q000139:chemically induced / Q000276:immunology / Q000503:physiopathology*; D016535:Bronchial Hyperreactivity / Q000139:chemically induced / Q000276:immunology* / Q000473:pathology; D001991:Bronchitis / Q000139:chemically induced / Q000276:immunology* / Q000473:pathology; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D004195:Disease Models, Animal; D004804:Eosinophils / Q000276:immunology* / Q000473:pathology; D005260:Female; D008168:Lung / Q000276:immunology* / Q000473:pathology; D016210:Methacholine Chloride / Q000633:toxicity; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000008:administration & dosage / Q000276:immunology*; D011657:Pulmonary Eosinophilia / Q000139:chemically induced / Q000276:immunology* / Q000473:pathology
D000336:Aerosols; D016210:Methacholine Chloride; D010047:Ovalbumin