This study examined the expression of the anterior gradient-2 （AGR2） protein and Muc5ac protein in the lung tissues of asthmatic mice and the effect of dexamethasone, with an at- tempt to explore the role of AGR2 in the over-secretion of mucus in the airway. Eighteen BALB/c mice were divided into asthma group, control group and dexamethasone group. In dexamethasone group, dexamethasone was intraperitoneally administered. Expression of AGR2 protein and Muc5ac protein in the murine lung tissues was immunohistochemically detected. IL-13 level was determined in the bronchoalveolar lavage fluid （BALF） by ELISA. The results exhibited that the expression of AGR2 protein in asthma group （0.522±0.041） was significantly higher than that in normal controls （0.361±0.047） （P〈0.01） and bore a positive linear relationship to the expression of Muc5ac protein （r=0.873, P〈0.05） and IL-13 level （r=0.828, P〈0.05）. Expression of AGR2 protein in the dexa- methasone group （0.456±0.049） was significantly lower than that in the asthma group. It was concluded that： （1） the expression of AGR2 protein was significantly higher in asthmatic mice as com- pared with their normal counterparts; （2） the expression was obviously related to the expression of Muc5ac protein and IL-13; （3） dexamethasone could down-regulate the expression of AGR2 protein. Our findings suggested that AGR2 might be involved in the over-secretion of mucus in the airway in asthma.
Asthma affects about 300 million people worldwide, placing an enormous strain on health resources inmany countries. Evidence is increasing that asthma is a complex condition with different underlying pathophysiologiesJ Scientists around the world have devoted much effort to unveiling this heterogeneity, from phenotyping initially focused on combinations of clinical characteristics, towards endotypes evolving which link pathophysiological mechanism to subtypes of asthma.2 The identification of these endotypes, either by matching biology, genetics and therapeutic responses with clinically defined phenotypes or through unbiased genomic approaches, remains limited.3 Moving forward, ongoing studies that expand on these insights into the molecular signatures should enhance our ability to define the endotypes and lead to more targeted approaches to asthma therapy.4
