The pathophysiology of chronic airflow obstruction, such as bronchial asthma, is characterized by mucus hypersecretion, goblet cell hyperplasia(GCH), smooth muscle hypertrophy, cells infiltration. In fatal asthma patients, one findings is mucus hypersecretion due to GCH. However, the mechanisms of GCH in these hypersecretory diseases remain still unknown. In this study, a rat model was rapidly induced with GCH by instillation of TiO2 intratracheally. We intend to confirm GCH and association of concomitant inflammatory cells infiltration and to observe the effect of potent antiinflammatory agent, that is dexamethasone, on GCH with inflammatroy cells.

Twenty-one-8-weeks-old male Sprague-Dawley rats were divided into three groups. Endotoxin-free water was instilled intratracheally in group 1(control) ; TiO₂ was instilled in the group 2 ; and dexamethasone was injected intraperitoneally to group 3 before TiO₂ instillation. After 120 hours, all rats were sacrificed, and trachea, bronchi, and lungs were resected respectively. These tissues were made as paraffin blocks and stained as PAS for goblet cells and Luna stain for eosinophils. We calculated the ratio of goblet cell to respiratory epithelium and number of infiltrated eosinophils from each tissue.

(1) Fraction of goblet cells was significantly increased in group 2 than in group 1 in the trachea and in the main bronchus. (10.19±11.33% vs 4.09±8.28%, p<0.01 and 34.09±23.91% vs 3.61±4.84%, p<0.01, respectively). (2) Eosinophils were significantly increased in the airway of group 2 than that of group 1. (5.43±3.84% vs 0.17±0.47 in trachea and 47.71±16.91 vs 2.71±1.96 in main bronchi). (3) There was significant difference in the decrease of goblet cells and eosinophils(r=0.719, p=0.001). (4) There was significant difference in the decrease of goblet cells after dexamethasone infection between group 2 and group 3 (p<0.01). Also, infiltration of eosinophils was suppressed by dexamethasone.

We made an animal model of TiO₂-induced goblet cell hyperplasia. GCH was observed mainly in the main bronchi with concomitant eosinophilic infiltration. Both goblet cell hyperplasia and eosinophilic infiltration were suppressed by dexamethasone. This animal model may serve as a useful tool in understanding of the mechanism of GCH in chronic airway diseases.