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Arsenic trioxide alleviates airway hyperresponsiveness and eosinophilia in a murine model of asthma
Arsenic trioxide alleviates airway hyperresponsiveness and eosinophilia in a murine model of asthma
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Arsenic trioxide alleviates airway hyperresponsiveness and eosinophilia in a murine model of asthma
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Arsenic trioxide alleviates airway hyperresponsiveness and eosinophilia in a murine model of asthma
Arsenic trioxide alleviates airway hyperresponsiveness and eosinophilia in a murine model of asthma

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Arsenic trioxide alleviates airway hyperresponsiveness and eosinophilia in a murine model of asthma
Arsenic trioxide alleviates airway hyperresponsiveness and eosinophilia in a murine model of asthma
Journal Article

Arsenic trioxide alleviates airway hyperresponsiveness and eosinophilia in a murine model of asthma

2010
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Overview
Asthma is one of the most common chronic airway inflammatory diseases. The clinical hallmarks of asthma include elevated serum levels of immunoglobulin E (IgE), eosinophilic inflammation and airway hyper-responsiveness (AHR). Arsenic trioxide (As 2 O 3 ) is considered a carcinogen; however, it has also been used to treat diseases, such as syphilis, in traditional Chinese and Western medicine. Today, As 2 O 3 is used as one of the standard therapies for acute promyelocytic leukemia (APL). Previous studies have indicated that As 2 O 3 can induce apoptosis in eosinophils. However, the effect of As 2 O 3 on asthma has not been investigated. We used ovalbumin (OVA)-immunized mice as a model for asthma and treated mice with As 2 O 3 at doses of 2.5 and 5 mg/kg. The mice were then monitored for OVA-specific IgE production, airway inflammatory cell infiltration and AHR. We found that administration of As 2 O 3 in OVA-immunized mice abrogated airway eosinophil recruitment by downregulating eotaxin expression but did not alter serum IgE or IL-5 levels in bronchoalveolar lavage fluid (BALF). Furthermore, the development of AHR and cellular infiltration into the airway were reduced by treating mice with As 2 O 3 . In vitro data suggested that low concentrations of As 2 O 3 could induce only a small degree of apoptosis in primary pulmonary cells but could significantly inhibit the secretion of eotaxin by these cells. These results indicate that the administration of As 2 O 3 to OVA-immunized mice can suppress lung allergic inflammatory responses. As 2 O 3 might therefore have therapeutic potential in treating allergic airway inflammatory diseases.