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Background: Neutrophil migration into the airways is a key process in neutrophilic asthma. Developmental endothelial locus‐1 (DEL‐1), an extracellular matrix protein, is a neutrophil adhesion inhibitor that attenuates neutrophilic inflammation. Methods: Levels of DEL‐1 were measured in exhaled breath condensate (EBC) and serum in asthma patients by ELISA. DEL‐1 modulation of neutrophil adhesion and transepithelial migration was examined in a co‐culture model in vitro. The effects of DEL‐1‐adenoviral vector‐mediated overexpression on ovalbumin/lipopolysaccharide (OVA/LPS)‐induced neutrophilic asthma were studied in mice in vivo. Results: DEL‐1 was primarily expressed in human bronchial epithelial cells and was decreased in asthma patients. Serum DEL‐1 concentrations were reduced in patients with severe asthma compared with normal subjects (567.1 ± 75.3 vs. 276.8 ± 29.36 pg/mL, p <.001) and were negatively correlated to blood neutrophils (r = −0.2881, p =.0384) and neutrophil‐to‐lymphocyte ratio (NLR) (r = −0.5469, p <.0001). DEL‐1 concentrations in the EBC of severe asthmatic patients (113.2 ± 8.09 pg/mL) were also lower than normal subjects (193.0 ± 7.61 pg/mL, p <.001) and were positively correlated with the asthma control test (ACT) score (r = 0.3678, p =.0035) and negatively related to EBC IL‐17 (r = −0.3756, p =.0131), myeloperoxidase (MPO) (r = −0.5967, p =.0055), and neutrophil elastase (NE) (r = −0.5488, p =.0009) expression in asthma patients. Neutrophil adhesion and transepithelial migration in asthma patients were associated with LFA‐1 binding to ICAM‐1 and inhibited by DEL‐1. DEL‐1 mRNA and protein expression in human bronchial epithelial cells were regulated by IL‐17. Exogenous DEL‐1 inhibited IL‐17‐enhanced neutrophil adhesion and migration. DEL‐1 expression was decreased while neutrophil infiltration was increased in the airway of a murine model of neutrophilic asthma. This was prevented by DEL‐1 overexpression. Conclusions: DEL‐1 down‐regulation leads to increased neutrophil migration across bronchial epithelial cells and is associated with neutrophilic airway inflammation in asthma. [ABSTRACT FROM AUTHOR]

A hydroponic experiment was conducted to investigate the effects of indole-3-acetic acid (IAA) on arsenic (As) uptake and antioxidative enzymes in fronds ofPteris creticavar.nervosa(As hyperaccumulator) andPteris ensiformis(non-hyperaccumulator). Plants were exposed to 2 mg L−1As(III), As(V) or dimethylarsinic acid (DMA) and IAA concentrations for 14 d. The biomass and total As in the plants significantly increased at 30 mg L−1IAA. Superoxide dismutase (SOD) activities significantly increased with IAA addition. Catalase (CAT) activities showed a significant increase inP. ensiformisexposed to three As species at 30 or 50 mg L−1IAA but varied inP. creticavar.nervosa. Peroxidase (POD) activities were unchanged inP. ensiformisexcept for a significant decrease at 50 mg L−1IAA under As(III) treatment. However, a significant increase was observed inP. creticavar.nervosaat 10 mg L−1IAA under As(III) or DMA treatment and at 50 mg L−1IAA under As(V) treatment. Under DMA stress, malondialdehyde contents in fronds ofP. creticavar.nervosashowed a significant decrease at 10 mg L−1IAA but remained unchanged inP. ensiformis. Therefore, IAA enhanced As uptake and frond POD activity inP. creticavar.nervosaunder As stress. [ABSTRACT FROM PUBLISHER]