PMID- 20495578
OWN - NLM
STAT- MEDLINE
DCOM- 20101008
LR  - 20211020
IS  - 2042-0226 (Electronic)
IS  - 1672-7681 (Print)
IS  - 1672-7681 (Linking)
VI  - 7
IP  - 5
DP  - 2010 Sep
TI  - Arsenic trioxide alleviates airway hyperresponsiveness and eosinophilia in a 
      murine model of asthma.
PG  - 375-80
LID - 10.1038/cmi.2010.26 [doi]
AB  - 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 (As2O3) is considered a carcinogen; however, it has also been used to 
      treat diseases, such as syphilis, in traditional Chinese and Western medicine. 
      Today, As2O3 is used as one of the standard therapies for acute promyelocytic 
      leukemia (APL). Previous studies have indicated that As2O3 can induce apoptosis 
      in eosinophils. However, the effect of As2O3 on asthma has not been investigated. 
      We used ovalbumin (OVA)-immunized mice as a model for asthma and treated mice 
      with As2O3 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 As2O3 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 As2O3. In vitro data suggested that low concentrations of 
      As2O3 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 As2O3 to OVA-immunized mice can 
      suppress lung allergic inflammatory responses. As2O3 might therefore have 
      therapeutic potential in treating allergic airway inflammatory diseases.
FAU - Chu, Kuan-Hua
AU  - Chu KH
AD  - Graduate Institute of Immunology, National Taiwan University, Taipei, Taiwan.
FAU - Lee, Chen-Chen
AU  - Lee CC
FAU - Hsin, Shao-Chi
AU  - Hsin SC
FAU - Cai, Bao-Chang
AU  - Cai BC
FAU - Wang, Jin-Hong
AU  - Wang JH
FAU - Chiang, Bor-Luen
AU  - Chiang BL
LA  - eng
PT  - Journal Article
DEP - 20100524
PL  - China
TA  - Cell Mol Immunol
JT  - Cellular & molecular immunology
JID - 101242872
RN  - 0 (Arsenicals)
RN  - 0 (Interleukin-5)
RN  - 0 (Oxides)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - S7V92P67HO (Arsenic Trioxide)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Arsenic Trioxide
MH  - Arsenicals/*therapeutic use
MH  - Asthma/blood/*drug therapy/*immunology/pathology
MH  - Bronchial Hyperreactivity/blood/*drug therapy/*immunology/pathology
MH  - Bronchoalveolar Lavage Fluid/immunology
MH  - Cells, Cultured
MH  - Disease Models, Animal
MH  - Eosinophils/*drug effects/*immunology
MH  - Female
MH  - Immunoglobulin E/blood
MH  - Interleukin-5/immunology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Oxides/*therapeutic use
PMC - PMC4002675
EDAT- 2010/05/25 06:00
MHDA- 2010/10/12 06:00
PMCR- 2010/09/01
CRDT- 2010/05/25 06:00
PHST- 2010/05/25 06:00 [entrez]
PHST- 2010/05/25 06:00 [pubmed]
PHST- 2010/10/12 06:00 [medline]
PHST- 2010/09/01 00:00 [pmc-release]
AID - cmi201026 [pii]
AID - 10.1038/cmi.2010.26 [doi]
PST - ppublish
SO  - Cell Mol Immunol. 2010 Sep;7(5):375-80. doi: 10.1038/cmi.2010.26. Epub 2010 May 
      24.